WO2024254542A1

WO2024254542A1 - Methods of treatment using an anti-abeta protofibril antibody

Info

Publication number: WO2024254542A1
Application number: PCT/US2024/033125
Authority: WO
Inventors: Shobha DHADDA; Steven Hersch; Michael Irizarry; Akihiko Koyama; Lynn Kramer; Larisa Reyderman; Pallavi SACHDEV; Brian Willis
Original assignee: Eisai R&D Management Co., Ltd.
Priority date: 2023-06-09
Filing date: 2024-06-07
Publication date: 2024-12-12

Abstract

Disclosed herein are methods of selecting, monitoring, and treating subjects with Alzheimer's disease (AD) or suspected of having AD or another disorder associated with amyloid accumulation in the brain based on the risk of an ARIA event or brain hemorrhage. Also disclosed herein are methods of treating subjects having or suspected of having AD comprising subcutaneously administering an anti-Aβ protofibril antibody.

Description

Attorney Docket No.08061.0062-00304 METHODS OF TREATMENT USING AN ANTI-Aβ PROTOFIBRIL ANTIBODY RELATED APPLICATIONS This application claims the benefit of and priority to US Provisional Application Serial No.63/507,400, filed June 9, 2023, US Provisional Application Serial No.63/572,110, filed March 29, 2024, and US Provisional Application Serial No.63/648,077, filed May 15, 2024, the contents of each of which are incorporated herein by reference in their entirety. FIELD Disclosed herein are methods and dosing regimens for treating Alzheimer’s disease (AD) in a subject with an anti-Aβ protofibril antibody, as well as methods relating to amyloid related imaging abnormalities (ARIA). BACKGROUND Alzheimer’s disease (AD) is a progressive, neurodegenerative disorder of unknown etiology and the most common form of dementia among older people. In 2006, there were 26.6 million cases of AD in the world (range: 11.4-59.4 million) (Brookmeyer, R., et al., Forecasting the global burden of Alzheimer’s Disease. Alzheimer Dement.2007; 3:186-91), while there were more than 5 million people in the United States reportedly living with AD (Alzheimer’s Association, Alzheimer’s Association report, 2010 Alzheimer’s disease facts and figures. Alzheimer Dement.2010; 6:158-94). By the year 2050, the worldwide prevalence of AD is predicted to grow to 106.8 million (range: 47.2-221.2 million), while in the United States alone the prevalence is estimated to be 11 to 16 million. (Brookmeyer, supra, and 2010 Alzheimer’s disease facts and figures, supra). The disease generally involves a global decline of cognitive function that progresses slowly and leaves end-stage subjects bedridden. AD subjects typically survive for only 3 to 10 years after symptom onset, although extremes of 2 and 20 years are known. (Hebert, L.E., et al., Alzheimer disease in the U.S. population: prevalence estimates using the 2000 census. Arch Neurol.2003; 60:1119-1122.) AD is the seventh leading cause of all deaths in the United States and the fifth leading cause of death in Americans older than the age of 65 years, despite the fact that mortality due to AD is greatly underestimated because death certificates rarely attribute the cause of death to AD. (Alzheimer’s Association. Alzheimer’s Association report.2010 Alzheimer’s disease facts and figures. Alzheimer Dement.2010; 6:158-94.) AD represents a significant economic burden across industrialized countries with a substantial impact on healthcare systems and the public purse as well as on subjects and their families. In the United States alone, total payments for 2010 were estimated at $172 billion, including $123 billion for Medicare and Medicaid. Attorney Docket No.08061.0062-00304 Histologically, the disease is characterized by neuritic plaques, found primarily in the association cortex, limbic system and basal ganglia. The major constituent of these plaques is amyloid beta peptide (Aβ). Aβ exists in various conformational states - monomers, oligomers, protofibrils, and insoluble fibrils. Details of the mechanistic relationship between onset of Alzheimer’s disease and Aβ production is unknown. However, some anti-Aβ antibodies are undergoing clinical study now as potential therapeutic agents for Alzheimer’s disease. Despite the recent development of treatments for AD, including those targeting Aβ, there remains a need for better treatments, including more refined methods of selecting patients suitable for treatment and calibrating responses to treatment events such as ARIA. Accordingly, disclosed herein are improved methods of selecting, monitoring, and treating patients with AD to treat patients less likely to exhibit ARIA and/or to address response to incidences of ARIA during treatment. SUMMARY One aspect of the present disclosure relates to a method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising subcutaneously administering to the subject 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg), of an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3). Another aspect of the present disclosure relates to a method of delaying clinical decline in a subject having AD, suspected of having AD, or at risk for AD, comprising subcutaneously administering to the subject 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg), of an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3). A further aspect of the present disclosure relates to a method of reducing brain amyloid level in a subject having AD, suspected of having AD, or at risk for AD, comprising subcutaneously administering to the subject 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg), of an antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID Attorney Docket No.08061.0062-00304 NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3). Another aspect of the present disclosure relates to a method of converting an amyloid positive subject to amyloid negative, comprising subcutaneously administering to the subject 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg), of an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3). In some embodiments, the anti-Aβ protofibril antibody is subcutaneously administered at 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg) reduces a biomarker of AD pathology and/or provides a lower systemic exposure (e.g., AUC) to the antibody than for a higher dose such as 720 mg administered subcutaneously. In some embodiments, the anti-Aβ protofibril antibody is subcutaneously administered at 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg) reduces a risk for developing ARIA relative to a higher dose of the antibody, such as 720 mg administered subcutaneously. In some embodiments, the anti-Aβ protofibril antibody is administered at a dose of 150 mg to 200 mg, 200 mg to 250 mg, 250 mg to 300 mg, 350 mg to 400 mg, 450 mg to 500 mg, or 550 mg to 600 mg. In some embodiments, the anti-Aβ protofibril antibody is administered subcutaneously at a dose of 500 mg. In some embodiments, the dose is administered in two parts, e.g., consecutively. In some embodiments, the anti-Aβ protofibril antibody is administered once weekly. In some embodiments, the anti-Aβ protofibril antibody is administered once biweekly. In some embodiments, the anti-Aβ protofibril antibody is administered once monthly. In some embodiments, the anti-Aβ protofibril antibody is administered at an initiation dose for a first time period, e.g., according to an initiation dosing regimen, and administered at a maintenance dose for a second time period, e.g., according to a maintenance dosing regimen. In some embodiments, the initiation dosing regimen comprises intravenous administration of each initiation dose or subcutaneous administration of each initiation dose. In some embodiments, the maintenance dosing regimen comprises subcutaneous administration of each maintenance dose or intravenous administration of each maintenance dose. Attorney Docket No.08061.0062-00304 In some embodiments, the initiation dosing regimen comprises at least one initiation dose administered intravenously and at least one initiation dose administered subcutaneously. In some embodiments, the maintenance dosing regimen comprises at least one maintenance dose administered intravenously and at least one maintenance dose administered subcutaneously. In some embodiments, the initiation dose is greater than the maintenance dose. In some embodiments, the initiation dose of the anti-Aβ protofibril antibody is 150 mg to 600 mg, e.g., 200 mg to 550 mg, preferably 500 mg, administered subcutaneously. In some embodiments, the maintenance dose of the anti-Aβ protofibril antibody is 150 mg to 500 mg, e.g., 360 mg, administered subcutaneously. In some embodiments, the maintenance dose of the anti-Aβ protofibril antibody is 250 mg administered subcutaneously. In some embodiments, the initiation dose is administered weekly. In some embodiments, the maintenance dose is administered weekly. In some embodiments, the maintenance dose is administered biweekly. In some embodiments, the first time period is at least about 6 months, about 12 months, about 18 months, about 24 months, or about 30 months. In some embodiments, the first time period is at least 18 months. In some embodiments, the first time period is at least 24 months. In some embodiments, the first time period lasts until the subject is amyloid negative. In some embodiments, the anti-Aβ protofibril antibody (e.g., BAN2401) is subcutaneously administered at an initiation dose of 500 mg weekly for at least 18 months and then subcutaneously administered at a maintenance dose of 250 mg weekly for the second period of time. In some embodiments, the anti-Aβ protofibril antibody (e.g., BAN2401) is subcutaneously administered at an initiation dose of 500 mg weekly for at least 24 months, and then subcutaneously administered at a maintenance dose of 250 mg biweekly for the second period of time. In some embodiments, the second time period begins when one or more biomarkers in the subject indicate a reduction in or slowing of AD progression. In some embodiments, the second time period is at least about 6 months, about 12 months, about 18 months, about 24 months, about 36 months, about 42 months, about 48 months, about 54 months, about 60 months, or for the lifetime of the subject. Attorney Docket No.08061.0062-00304 In some embodiments, the maintenance dose is subcutaneously administered with an autoinjector (AI). In some embodiments, the anti-Aβ protofibril antibody is intravenously administered at a dose of 10 mg/kg relative to the weight of the subject, biweekly. In some embodiments, the anti-Aβ protofibril antibody is comprised in a pharmaceutical composition in the form of a pre-filled syringe. In some embodiments, the anti-Aβ protofibril antibody is comprised in a pharmaceutical composition via an autoinjector. In some embodiments, the anti-Aβ protofibril antibody comprising a heavy chain complementarity variable region comprising an amino acid sequence of SEQ ID NO: 1, and a light chain variable region comprising an amino acid sequence of SEQ ID NO: 2. In some embodiments, the anti-Aβ protofibril antibody is BAN2401 (lecanemab). In some embodiments, the subject shows a change and/or difference in a measurement of one or more biomarkers associated with AD pathology prior to treatment. In some embodiments, the change and/or difference in the measurement is selected from: a. increased amyloid in the brain, e.g., as measured by amyloid PET (e.g., a centiloid measure of about 20-40, e.g., a centiloid measure of about 20-32), b. increased tau in the brain, e.g., as measured by positron emission tomography (PET), c. decreased cerebrospinal fluid levels of ratio of Aβ1-42/1- 40 and/or increased total tau, p-tau (e.g., p-tau181, p-tau217, and/or p-tau231), the ratio of p- tau181/np-tau181, the ratio of p-tau217/np-tau217), neurogranin, and/or neurofilament light chain (NfL), and d. decreased blood serum or plasma levels of a ratio of Aβ1-42/1-40 and/or increased total tau, phosphorylated tau (P-tau) isoforms (e.g., P-tau181, P-tau217, and/or P-tau231), ratio of p- tau181/np-tau181, the ratio of p-tau217/np-tau217, glial fibrillary acidic protein (GFAP), and/or neurofilament light chain (NfL). In some embodiments, the subject shows a change and/or difference in a measurement of one or more biomarkers associated with AD pathology during and/or after treatment. In some embodiments, the change and/or difference in the measurement is selected from: a. decreased amyloid in the brain, e.g., as measured by amyloid PET (e.g., a centiloid measure of about 20-40, e.g., a centiloid measure of about 20-32), b. decreased tau in the brain, e.g., as measured by positron emission tomography (PET), c. increased cerebrospinal fluid levels of ratio of Aβ1-42/1- 40 and/or decreased total tau, p-tau (e.g., p-tau181, p-tau217, and/or p-tau231, the ratio of p- tau181/np-tau181, the ratio of p-tau217/np-tau217), neurogranin, and/or neurofilament light chain (NfL), and d. increased blood serum or plasma levels of a ratio of Aβ1-42/1-40 and/or decreased total Attorney Docket No.08061.0062-00304 tau, phosphorylated tau (P-tau) isoforms (e.g., P-tau181, P-tau217, and/or P-tau231), ratio of p- tau181/np-tau181, the ratio of p-tau217/np-tau217, glial fibrillary acidic protein (GFAP), and/or neurofilament light chain (NfL). In some embodiments, the subject is amyloid-positive prior to administration, e.g., as indicated by a PET assessment, a CSF assessment of Aβ(1-42), a CSF assessment of total tau, a CSF assessment of p-tau (e.g., p-tau181, p-tau217, and/or p-tau231, the ratio of p-tau181/np-tau181, and/or the ratio of p-tau217/np-tau217), MRI, retinal amyloid accumulation, and/or a blood biomarker assessment (e.g. a plasma Aβ1-42/1-40 ratio, plasma p-tau181, plasma p-tau217, plasma p-tau 231 level, the ratio of p-tau181/np-tau181, and/or the ratio of p-tau217/np-tau217). In some embodiments, the subject is ApoE4-positive. In some embodiments, the subject is monitored for development of ARIA. In some embodiments, the subject is 65 to 80 years old. In some embodiments, the subject is 55 to 64 years old and has at least one risk factor chosen from: (i) a first degree relative diagnosed with dementia onset before age 75; (ii) at least one apolipoprotein E4 variant (APOE4) allele; and (iii) elevated brain amyloid according to PET or cerebrospinal fluid (CSF) testing prior to said administration. In some embodiments, the subject has Alzheimer’s disease. In some embodiments, the subject has early Alzheimer’s disease. In some embodiments, the subject has been diagnosed with a. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood and/or has been diagnosed as having mild Alzheimer’s disease dementia; b. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by National Institute of Aging – Alzheimer’s Association (NIA-AA) core clinical criteria; c. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by a CDR global score of 0.5 and a Memory Box score of 0.5 or greater before treatment; d. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by a history of subjective memory decline with gradual onset and slow progression over the last 1 year before treatment, e.g., as corroborated by an informant; e. mild Alzheimer’s disease dementia by the NIA-AA core clinical criteria for probable Alzheimer’s disease dementia; or f. mild Alzheimer’s disease dementia by a CDR score of 0.5 to 1.0 and a Memory Box score of 0.5 or greater before treatment. In some embodiments, the subject is suspected of having AD. In some embodiments, the subject is a subject at risk for developing AD. In some embodiments, the subject at risk for developing AD has pre-AD. In some embodiments, the subject does not have cognitive impairment. Attorney Docket No.08061.0062-00304 In some embodiments, the subject has a Global Clinical Dementia Rating (CDR) score of 0 at prior to said administration. In some embodiments, the subject has a Mini-Mental State Examination (MMSE) score greater than or equal to 27, with educational adjustments, prior to said administration. In some embodiments, the subject has a Wechsler Memory Scale-Revised Logical Memory subscale II (WMS-R LM II) score prior to said administration of at least one standard deviation below age-adjusted mean in the WMS-IV LMII of less than or equal to 15 for a subject of age ranging from 50 to 64 years, of less than or equal to 12 for a subject of age ranging from 65 to 69 years, of less than or equal to 11 for a subject of age ranging from 70 to 74 years, of less than or equal to 9 for a subject of age ranging from 75 to 79 years, and of less than or equal to 7 for a subject of age ranging from 80 to 90 years. An aspect of the present disclosure relates to a method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the antibody biweekly at an initiation dose of 10 mg/kg relative to the weight of the subject; and subcutaneously administering, e.g., after 18 or 24 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg. One aspect of the present disclosure relates to a method of delaying clinical decline in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the antibody biweekly at an initiation dose of 10 mg/kg relative to the weight of the subject; and subcutaneously administering, e.g., after 18 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg. Another aspect of the present disclosure relates to a method of reducing brain amyloid level in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to Attorney Docket No.08061.0062-00304 the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the antibody biweekly at an initiation dose of 10 mg/kg relative to the weight of the subject; and subcutaneously administering, e.g., after 18 or 24 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg. A further aspect of the present disclosure relates to a method of converting an amyloid positive subject to amyloid negative comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3) , according to a dosage regimen comprising: intravenously administering the antibody biweekly at an initiation dose of 10 mg/kg relative to the weight of the subject; and subcutaneously administering, e.g., after 18 or 24 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg. In some embodiments, the initiation dose of the antibody is administered intravenously for at least 6 months, at least 12 months, at least 18 months, or at least 24 months. In some embodiments, the initiation dose of the antibody is administered intravenously for at least 18 months. In some embodiments, the initiation dose of the antibody is administered intravenously for at least 24 months. In some embodiments, the maintenance dose of the antibody is administered weekly. In some embodiments, the maintenance dose of the antibody is administered biweekly. In some embodiments, the maintenance dose of the antibody is administered using a vial- syringe. In some embodiments, the maintenance dose of the antibody is administered using an AI. One aspect of the present disclosure relates to a method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity Attorney Docket No.08061.0062-00304 determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: subcutaneously administering the antibody weekly at an initiation dose of 500 mg; and subcutaneously administering, e.g., after 18 or 24 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg. Another aspect of the present disclosure relates to a method of delaying clinical decline in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: subcutaneously administering the antibody weekly at an initiation dose of 500 mg; and subcutaneously administering, e.g., after 18 or 24 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg. A further aspect of the present disclosure relates to a method of reducing brain amyloid level in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: subcutaneously administering the antibody weekly at an initiation dose of 500 mg; and subcutaneously administering, e.g., after 18 or 24 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg. Another aspect of the present disclosure relates to a method of converting an amyloid positive subject to amyloid negative comprising administering to the subject an antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3) , according to a dosage regimen comprising: subcutaneously administering Attorney Docket No.08061.0062-00304 the antibody weekly at an initiation dose of 500 mg; and subcutaneously administering, e.g., after 18 or 24 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg. In some embodiments, the initiation dose of the antibody is administered subcutaneously for at least 6 months, at least 12 months, at least 18 months, or at least 24 months. In some embodiments, the initiation dose of the antibody is administered subcutaneously for at least 18 months. In some embodiments, the initiation dose of the antibody is administered subcutaneously for at least 24 months. In some embodiments, the initiation dose of the antibody is administered using a vial- syringe. In some embodiments, the initiation dose of the antibody is administered using an AI. In some embodiments, the maintenance dose of the antibody is administered weekly. In some embodiments, the maintenance dose of the antibody is administered biweekly. In some embodiments, the maintenance dose of the antibody is administered using a vial- syringe. In some embodiments, the maintenance dose of the antibody is administered using an AI. In some embodiments, the anti-Aβ protofibril antibody comprising a heavy chain complementarity variable region comprising an amino acid sequence of SEQ ID NO: 1, and a light chain variable region comprising an amino acid sequence of SEQ ID NO: 2. In some embodiments, the anti-Aβ protofibril antibody is BAN2401 (lecanemab). In some embodiments, the subject shows a change in a measurement of one or more biomarkers associated with AD pathology prior to treatment. In some embodiments, the change in the measurement is selected from: a. increased amyloid in the brain, e.g., as measured by amyloid PET (e.g., a centiloid measure of about 20-40, e.g., a centiloid measure of about 20-32), b. increased tau in the brain, e.g., as measured by positron emission tomography (PET), c. decreased cerebrospinal fluid levels of a ratio of Aβ1-42/1-40, and/or increased total tau, p-tau (e.g, p-tau181, p-tau217, and/or p-tau231), ratio of p-tau181/np-tau181, ratio of p-tau217/np-tau217, neurogranin, and/or neurofilament light chain (NfL), and d. decreased blood serum or plasma levels of a ratio of Aβ1-42/1-40 and/or increased total tau, phosphorylated tau (P- tau) isoforms (e.g., P-tau181, P-tau217, and/or P-tau231, ratio of p-tau181/np-tau181, ratio of p- tau217/np-tau217, glial fibrillary acidic protein (GFAP), and/or neurofilament light chain (NfL). Attorney Docket No.08061.0062-00304 In some embodiments, the subject shows a change and/or difference in a measurement of one or more biomarkers associated with AD pathology during and/or after treatment. In some embodiments, the change and/or difference in the measurement is selected from: a. decreased amyloid in the brain, e.g., as measured by amyloid PET (e.g., a centiloid measure of about 20-40, e.g., a centiloid measure of about 20-32), b. decreased tau in the brain, e.g., as measured by positron emission tomography (PET), c. increased cerebrospinal fluid levels of ratio of Aβ1-42/1- 40 and/or decreased total tau, p-tau (e.g., p-tau181, p-tau217, and/or p-tau231, the ratio of p- tau181/np-tau181, and/or the ratio of p-tau217/np-tau217), neurogranin, and/or neurofilament light chain (NfL), and d. increased blood serum or plasma levels of a ratio of Aβ1-42/1-40 and/or decreased total tau, phosphorylated tau (P-tau) isoforms (e.g., P-tau181, P-tau217, and/or P-tau231), ratio of p-tau181/np-tau181, the ratio of p-tau217/np-tau217, glial fibrillary acidic protein (GFAP), and/or neurofilament light chain (NfL). In some embodiments, the subject is amyloid-positive prior to administration, e.g., as indicated by a PET assessment, a CSF assessment of Aβ(1-42), MRI, retinal amyloid accumulation. In some embodiments, the subject is ApoE4-positive. In some embodiments, the subject is monitored for development of ARIA. In some embodiments, the subject is 65 to 80 years old. In some embodiments, the subject is 55 to 64 years old and has at least one risk factor chosen from: (i) a first degree relative diagnosed with dementia onset before age 75; (ii) at least one apolipoprotein E4 variant (APOE4) allele; and (iii) elevated brain amyloid according to PET or cerebrospinal fluid (CSF) testing prior to said administration. In some embodiments, the subject has Alzheimer’s disease. In some embodiments, the subject has early Alzheimer’s disease. In some embodiments, the subject has been diagnosed with a. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood and/or has been diagnosed as having mild Alzheimer’s disease dementia; b. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by National Institute of Aging – Alzheimer’s Association (NIA-AA) core clinical criteria; c. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by a CDR global score of 0.5 and a Memory Box score of 0.5 or greater before treatment; d. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by a history of subjective memory decline with gradual onset and slow progression over the last 1 year before treatment, e.g., as corroborated by an informant; e. mild Alzheimer’s disease dementia by the NIA-AA core clinical Attorney Docket No.08061.0062-00304 criteria for probable Alzheimer’s disease dementia; or f. mild Alzheimer’s disease dementia by a CDR score of 0.5 to 1.0 and a Memory Box score of 0.5 or greater before treatment. In some embodiments, the subject is suspected of having AD. In some embodiments, the subject is a subject at risk for developing AD. In some embodiments, the subject at risk for developing AD has pre-AD. In some embodiments, the subject does not have cognitive impairment. In some embodiments, the subject has a Global Clinical Dementia Rating (CDR) score of 0 at prior to said administration. In some embodiments, the subject has a Mini-Mental State Examination (MMSE) score greater than or equal to 27, with educational adjustments, prior to said administration. In some embodiments, the subject has a Wechsler Memory Scale-Revised Logical Memory subscale II (WMS-R LM II) score prior to said administration of at least one standard deviation below age-adjusted mean in the WMS-IV LMII of less than or equal to 15 for a subject of age ranging from 50 to 64 years, of less than or equal to 12 for a subject of age ranging from 65 to 69 years, of less than or equal to 11 for a subject of age ranging from 70 to 74 years, of less than or equal to 9 for a subject of age ranging from 75 to 79 years, and of less than or equal to 7 for a subject of age ranging from 80 to 90 years. A further aspect of the present disclosure relates to a method of treating a subject having early AD, suspected of having early AD, or at risk for early AD, and who has received a first anti-Aβ antibody, comprising: administering to the subject a second anti-Aβ antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the second antibody biweekly or monthly at a maintenance dose of 10 mg/kg relative to the weight of the subject; or subcutaneously administering the second antibody weekly or biweekly at a maintenance dose of 250 mg. Another aspect of the present disclosure relates to a method of delaying clinical decline in a subject who has received a first anti-Aβ antibody, comprising: administering to the subject a second anti-Aβ antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions Attorney Docket No.08061.0062-00304 (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the second antibody biweekly or monthly at a maintenance dose of 10 mg/kg relative to the weight of the subject; or subcutaneously administering the second antibody weekly or biweekly at a maintenance dose of 250 mg. One aspect of the present disclosure relates to a method of reducing a brain amyloid level in a subject in a subject who has received a first anti-Aβ antibody, comprising: administering to the subject a second anti-Aβ antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the second antibody biweekly or monthly at a maintenance dose of 10 mg/kg relative to the weight of the subject; or subcutaneously administering the second antibody weekly or biweekly at a maintenance dose of 250 mg. A further aspect of the present disclosure relates to a method of maintaining amyloid levels in a subject who has received a first anti-Aβ antibody, comprising: administering to the subject a second anti-Aβ antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3) , according to a dosage regimen comprising: intravenously administering the second antibody biweekly or monthly at a maintenance dose of 10 mg/kg relative to the weight of the subject; or subcutaneously administering the second antibody weekly or biweekly at a maintenance dose of 250 mg. One aspect of the present disclosure relates to a method of treating a subject having early AD, suspected of having early AD, or at risk for early AD, comprising: administering to the subject a first anti-Aβ antibody, administering to the subject a second anti-Aβ antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the second antibody biweekly or monthly at a maintenance dose of 10 mg/kg relative to the weight of the subject; Attorney Docket No.08061.0062-00304 or subcutaneously administering the second antibody weekly or biweekly at a maintenance dose, of 250 mg. In some embodiments, the subcutaneously administered maintenance dose of the antibody is administered using a vial-syringe. In some embodiments, the subcutaneously administered maintenance dose of the antibody is administered using an AI. In some embodiments, the first anti-Aβ antibody is selected from aducanumab, bapineuzumab, crenezumab, donanemab, gantenerumab, lecanemab, or solanezumab. In some embodiments, the first anti-Aβ antibody is donanemab. Another aspect of the present disclosure relates to a method of treating a subject having early AD, suspected of having early AD, or at risk for early AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the antibody biweekly at a first initiation dose of 10 mg/kg relative to the weight of the subject; subcutaneously administering the antibody weekly at a second initiation dose of 720 or 500 mg; and subcutaneously administering, e.g., after 18 or 24 months of treatment on the initiation doses, the antibody weekly at a dose of 250 mg. In some embodiments, the subject is on a thrombolytic or anti-platelet agent but not an anticoagulant. In some embodiments, the subject is receiving an anti-platelet medication. In some embodiments, the subject is receiving a thrombolytic agent. In some embodiments, the thrombolytic agent selected from the group of aspirin or a fibrinolytic agent. In some embodiments, the subject is receiving aspirin. In some embodiments, the subject is receiving a fibrinolytic. In some embodiments, the subject has had or is at an increased risk for a brain hemorrhage event, e.g., a microhemorrhage or intracerebral hemorrhage, or an ARIA event, prior to treatment. In some embodiments, the subject has not had a brain hemorrhage event, e.g., a microhemorrhage or intracerebral hemorrhage, or an ARIA event, prior to treatment. Attorney Docket No.08061.0062-00304 Enumerated Embodiments 1. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject a therapeutically effective dose of an anti-amyloid β (Aβ) protofibril antibody, wherein the subject does not have a brain hemorrhage event, e.g., a microhemorrhage or intracerebral hemorrhage, prior to treatment and/or wherein the subject has not exhibited a change, e.g., a decrease in brain white matter as measured by brain imaging prior to the treatment. 2. A method of selecting a subject having AD, suspected of having AD, or at risk for AD, for treatment with an anti-amyloid β (Aβ) protofibril antibody, comprising: a. determining that the subject has not had and/or does not currently have a brain hemorrhage event, e.g., a microhemorrhage or intracerebral hemorrhage, and/or has not exhibited a change, e.g., a decrease, in brain white matter as measured by brain imaging prior to the treatment; b. selecting the subject for treatment with a therapeutically effective dose of the anti-amyloid β (Aβ) protofibril antibody. 3. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject a therapeutically effective dose of an anti-amyloid β (Aβ) protofibril antibody, wherein the subject is on a thrombolytic or anti-platelet agent but not an anticoagulant. 4. The method of embodiment 3, wherein the subject is receiving an anti-platelet medication. 5. The method of embodiment 3, wherein the subject is receiving a thrombolytic agent. 6. The method of embodiment 5, wherein the thrombolytic agent selected from the group of aspirin or a fibrinolytic agent. 7. The method of embodiment 6, wherein the subject is receiving aspirin. 8. The method of embodiment 6, wherein the subject is receiving a fibrinolytic. 9. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject a therapeutically effective dose of an anti-amyloid β (Aβ) protofibril antibody, wherein the subject is not treated with an anticoagulant. 10. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject a therapeutically effective dose of an anti-amyloid β (Aβ) protofibril antibody, wherein the subject is at an increased risk of an ARIA event or brain hemorrhage event, e.g., a microhemorrhage or intracerebral hemorrhage, the method further comprising administering a steroid and/or monitoring the subject’s brain (e.g., by MRI). Attorney Docket No.08061.0062-00304 11. The method of embodiment 10, wherein the subject has had a brain hemorrhage event, e.g., a microhemorrhage or intracerebral hemorrhage, or an ARIA event prior to treatment. 12. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject a therapeutically effective dose of an anti-amyloid β (Aβ) protofibril antibody, detecting an ARIA event, e.g., a severe ARIA event, ARIA- H, ARIA-E, and administering a steroid. 13. The method of any one of embodiments 1-12, wherein the method reduces brain amyloid. 14. A method of treating severe ARIA in a subject receiving an anti-amyloid β (Aβ) protofibril antibody, the method comprising administering a steroid and/or monitoring the subject’s brain (e.g., by MRI). 15. The method of any one of embodiments 1-14, wherein the anti-Aβ protofibril antibody comprises three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 1 (HCDR1), SEQ ID NO: 2 (HCDR2), and SEQ ID NO: 3 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 4 (LCDR1), SEQ ID NO: 5 (LCDR2), and SEQ ID NO: 6 (LCDR3). 16. The method of any one of embodiments 1-15, wherein the anti-Aβ protofibril antibody comprises a heavy chain variable region comprising an amino acid sequence of SEQ ID NO: 7 and a light chain variable region comprising an amino acid sequence of SEQ ID NO: 8. 17. The method of any one of embodiments 1-16, wherein the anti-Aβ protofibril antibody comprises BAN2401 (lecanemab). 18. The method of any one of embodiments 1-17, wherein the therapeutically effective dose of the anti-Aβ protofibril antibody comprises an intravenous infusion of 10 mg/kg relative to the weight of the subject. 19. The method of any one of embodiments 1-17, wherein the therapeutically effective dose of the anti-Aβ protofibril antibody comprises a subcutaneous administration of about 250 to 720 mg. 20. The method of any one of embodiments 1-17, wherein the therapeutically effective dose of the anti-Aβ protofibril antibody comprises a subcutaneous administration of 250 mg. 21. The method of any one of embodiments 1-17, wherein the therapeutically effective dose of the anti-Aβ protofibril antibody comprises a subcutaneous administration of 360 mg. 22. The method of any one of embodiments 1-17, wherein the therapeutically effective dose of the anti-Aβ protofibril antibody comprises a subcutaneous administration of 500 mg. Attorney Docket No.08061.0062-00304 23. The method of any one of embodiments 1-17, wherein the therapeutically effective dose of the anti-Aβ protofibril antibody comprises a subcutaneous administration of 720 mg. 24. The method of any one of embodiments 1-19, wherein the therapeutically effective dose is administered subcutaneously by an autoinjector. 25. The method of any one of embodiments 1-18, wherein the therapeutically effective dose is administered weekly. 26. The method of any one of embodiments 1-17 and 19-24, wherein the therapeutically effective dose is administered every 2 weeks. 27. The method of any one of embodiments 1-26, wherein the frequency of administration is reduced after 18 months of treatment, e.g., to a frequency of every 2, 4, 6, 8, 10, or 12 weeks. 28. The method of any one of embodiments 1-27, wherein the therapeutically effective dose is reduced after 18 months of treatment, e.g., to a dose of 360 mg administered subcutaneously, or 250 mg administered subcutaneously, or maintained at a dose of 10 mg/kg administered intravenously. 29. The method of any one of embodiments 22 or 24-28, wherein the therapeutically effective dose is reduced from a weekly dose of 500 mg administered subcutaneously to a weekly dose of 360 mg administered subcutaneously, or 250 administered subcutaneously. 30. The method of any one of embodiments 24-28, wherein the therapeutically effective dose is reduced from a weekly dose of 720 mg administered subcutaneously to a weekly dose of 360 mg administered subcutaneously, or 250 administered subcutaneously 31. The method of any one of embodiments 1-30, wherein the subject is sequentially or simultaneously administered a second therapeutic agent. 32. The method of embodiment 31, wherein the second therapeutic agent is an anti-tau antibody. 33. The method of embodiment 32, wherein the anti-tau antibody comprises three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO:15 (HCDR1), SEQ ID NO:16 (HCDR2), SEQ ID NO:17 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO:18 (LCDR1), SEQ ID NO:19 (LCDR2), and SEQ ID NO:20 (LCDR3). 34. The method of embodiment 32 or 33, wherein the anti-tau antibody or antigen binding fragment thereof comprises a heavy chain variable region of SEQ ID NO: 21 and a light chain variable region of SEQ ID NO: 22. 35. The method of any one of embodiments 1-34, wherein the method further comprises monitoring for ARIA, e.g., ARIA-E and/or ARIA-H, e.g., as observed by MRI. Attorney Docket No.08061.0062-00304 36. The method of any one of the embodiments 1-35, wherein the method does not require a titration step prior to administering to the subject a first therapeutically effective dose of the anti-Aβ protofibril antibody. 37. The method of any one of embodiments 1-36, wherein the method results in: a. an improvement or slowing of worsening of one or more cerebrospinal fluid biomarkers, e.g., Aβ1-42, Aβ1-40 (including a ratio of Aβ1-42 to Aβ1-40), total tau, p-tau (e.g., p-tau181, p-tau217, and/or p-tau231), the ratio of p-tau181/np-tau181, the ratio of p-tau217/np-tau217, neurogranin, neurofilament light (NfL) peptide, phosphorylated tau; and/or b. a reduction or a slowing of increase of plasma or serum biomarkers, e.g., Aβ1-42, Aβ1-40 (including a ratio of Aβ1-42 to Aβ1-40), total tau, phosphorylated tau (P-tau) (including tau phosphorylated at 181 (P-tau181), 217 (P-tau217), 231 (P-tau231)), the ratio of P-tau181/NP- tau181, and/or the ratio of P-tau217/NP-tau217, glial fibrillary acidic protein (GFAP), and/or neurofilament light (NfL); as compared to before treatment and/or as compared to an untreated control subject. 38. The method of any one of embodiments 1-37, wherein the treatment a. delays clinical decline as determined by ADCOMS; b. delays clinical decline as determined by ADAS MCI-ADL; c. delays clinical decline as determined by modified iADRS; d. delays clinical decline as measured by a CDR-SB; or e. delays clinical decline as measured by an ADAS-Cog. 39. The method of embodiment 37 or embodiment 38, wherein the result is measured at least 6 months after administration of a first therapeutically effective dose. 40. The method of any one of embodiments 37-39, wherein the result is measured at least 12 months after administration of a first therapeutically effective dose. 41. The method of any one of embodiments 37-39, wherein the result is measured at least 13 months after administration of a first therapeutically effective dose. 42. The method of any one of embodiments 37-39, wherein the result is measured at least 18 months after administration of a first therapeutically effective dose. 43. The method of any one of embodiments 37-42, wherein the subject is switched from an initiation dosing regimen to a maintenance dosing regimen. Attorney Docket No.08061.0062-00304 44. The method of embodiment 43, wherein the switch to a maintenance dose occurs after at least 6 months (e.g., 6 months, or 13 months, or 18 months) following the start of the initiation dosing regimen or after the subject has converted to amyloid negative status, e.g., as determined by an improvement in a biomarker. 45. The method of embodiment 43 or embodiment 44, wherein the initiation dosing regimen comprises an intravenous infusion at a therapeutically effective dose of 10 mg/kg relative to the weight of the subject every two weeks. 46. The method of embodiment 43 or 44, wherein the initiation dosing regimen comprises administering the anti-Aβ protofibril antibody subcutaneously at a therapeutically effective dose of 720 mg. 47. The method of embodiment 43 or 44, wherein the initiation dosing regimen comprises administering the anti-Aβ protofibril antibody subcutaneously at a therapeutically effective dose of 500 mg. 48. The method of any one of embodiments 43-47, wherein the maintenance dosing regimen comprises an intravenous infusion at a therapeutically effective dose of 10 mg/kg relative to the weight of the subject every month. 49. The method of any one of embodiments 43-47, wherein the maintenance dosing regimen comprises administering the anti-Aβ protofibril antibody subcutaneously at a therapeutically effective dose of 360 mg. 50. The method of any one of embodiments 43-47, wherein the maintenance dosing regimen comprises administering the anti-Aβ protofibril antibody subcutaneously at a therapeutically effective dose of 250 mg weekly. 51. The method of any one of embodiments 43-45, wherein the maintenance dosing regimen comprises the same dosing regimen as the initiation dosing regimen. 52. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising selecting a patient who is not on an anticoagulant and administering to the subject a therapeutically effective dose of an anti-amyloid β (Aβ) protofibril antibody. 53. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising selecting a patient who is not on a thrombolytic agent and administering to the subject a therapeutically effective dose of an anti-amyloid β (Aβ) protofibril antibody. 54. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising selecting a patient who is on an anticoagulant or a thrombolytic Attorney Docket No.08061.0062-00304 agent (e.g., aspirin, fibrinolytic), administering to the subject a therapeutically effective dose of an anti-amyloid β (Aβ) protofibril antibody, and monitoring for ARIA in said patient. 55. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject a therapeutically effective dose of an anti-amyloid β (Aβ) protofibril antibody, administering an anticoagulant or a thrombolytic agent (e.g., aspirin, fibrinolytic, antiplatelet) if needed, and monitoring the subject for ARIA. 56. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising: a. administering to the subject a therapeutically effective dose of an anti-amyloid β (Aβ) protofibril antibody; b. stopping administration of the anti-amyloid β (Aβ) protofibril antibody to the subject when administering an anticoagulant or a thrombolytic agent (e.g., aspirin, fibrinolytic, antiplatelet) to the subject; c. resuming administration of the anti-amyloid β (Aβ) protofibril antibody to the subject at or after the time that the anticoagulant or a thrombolytic agent (e.g., aspirin, fibrinolytic, antiplatelet) is no longer being administered to the subject, and d. monitoring the subject for ARIA. 57. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising selecting a patient who is on an anticoagulant or a thrombolytic agent (e.g., aspirin, fibrinolytic, antiplatelet) and delaying administration of an anti-amyloid β (Aβ) protofibril antibody to the subject until treatment with said anticoagulant or said thrombolytic agent has ended. 58. The method of any one of embodiments 1-57, wherein the subject shows a change and/or a difference in a measurement of one or more biomarkers associated with AD pathology prior to treatment as compared to a reference measurement (e.g., measurement from a healthy control). 59. The method of embodiment 58, wherein the change in the measurement is selected from: a. increased amyloid in the brain, e.g., as measured by amyloid PET (e.g., a centiloid measure of about 20-40, e.g., a centiloid measure of about 20-32), b. increased tau in the brain, e.g., as measured by positron emission tomography (PET), c. decreased cerebrospinal fluid levels of a ratio of Aβ1-42/1-40 and/or increased total tau, p- tau (e.g., p-tau181, p-tau217, p-tau231, the ratio of p-tau181/np-tau181, and/or the ratio of p- tau217/np-tau217), neurogranin, and/or neurofilament light chain (NfL), and Attorney Docket No.08061.0062-00304 d. decreased blood serum or plasma levels of a ratio of Aβ1-42/1-40 and/or increased total tau, phosphorylated tau (P-tau) isoforms (e.g., P-tau181, P-tau217, P-tau231, the ratio of P- tau181/NP-tau181, and/or the ratio of P-tau217/NP-tau217), glial fibrillary acidic protein (GFAP), and/or neurofilament light chain (NfL). 60. The method of any one of embodiments 1-59, wherein the subject is amyloid-positive prior to treatment, e.g., as indicated by a PET assessment, a CSF assessment of Aβ(1-42), MRI, retinal amyloid accumulation, and/or a blood biomarker assessment (e.g. an Aβ1-42/1-40 ratio, plasma p- tau181, plasma p-tau217, plasma p-tau 231 level, the ratio of p-tau181/np-tau181, and/or the ratio of p-tau217/np-tau217). 61. The method of any one of embodiments 1-60, wherein the subject is ApoE4-positive. 62. The method of any one of embodiments 1-61, wherein the subject is monitored for development of ARIA. 63. The method of any one of embodiments 1-62, wherein the subject is 65 to 80 years old. 64. The method of any one of embodiments 1-62, wherein the subject is 55 to 64 years old and has at least one risk factor chosen from: (i) a first degree relative diagnosed with dementia onset before age 75; (ii) at least one apolipoprotein E4 variant (APOE4) allele; and (iii) elevated brain amyloid according to PET or cerebrospinal fluid (CSF) testing prior to said administration. 65. The method of any one of embodiments 1-64, wherein the subject has Alzheimer’s disease. 66. The method of any one of embodiments 1-65, wherein the subject has early Alzheimer’s. 67. The method of any one of embodiments 1-66, wherein the subject has been diagnosed with a. mild cognitive impairment due to Alzheimer’s disease – intermediate likelihood and/or has been diagnosed as having mild Alzheimer’s disease dementia.; b. mild cognitive impairment due to Alzheimer’s disease – intermediate likelihood by National Institute of Aging – Alzheimer’s Association (NIA-AA) core clinical criteria; c. mild cognitive impairment due to Alzheimer’s disease – intermediate likelihood by a CDR global score of 0.5 and a Memory Box score of 0.5 or greater before treatment; d. mild cognitive impairment due to Alzheimer’s disease – intermediate likelihood by a history of subjective memory decline with gradual onset and slow progression over the last 1 year before treatment, e.g., as corroborated by an informant; Attorney Docket No.08061.0062-00304 e. mild Alzheimer’s disease dementia by the NIA-AA core clinical criteria for probable Alzheimer’s disease dementia; or f. mild Alzheimer’s disease dementia by a CDR score of 0.5 to 1.0 and a Memory Box score of 0.5 or greater before treatment. 68. The method of any one of embodiments 1-67, wherein the subject is suspected of having AD 69. The method of any one of embodiments 1-68, wherein the subject is a subject at risk for developing AD. 70. The method of embodiment 69, wherein the subject at risk for developing AD has pre- Alzheimer’s disease (pre-AD). 71. The method of embodiment 69 or embodiment 70, wherein the subject does not have cognitive impairment. 72. The method of any one of embodiments 69-71, wherein the subject has a Global Clinical Dementia Rating (CDR) score of 0 73. The method of any one of embodiments 69-72, wherein the subject has a Mini-Mental State Examination (MMSE) score greater than or equal to 27, with educational adjustments, prior to said administration. 74. The method of any one of embodiments 69-73, wherein the subject has a Wechsler Memory Scale-Revised Logical Memory subscale II (WMS-R LM II) score prior to said administration of at least one standard deviation below age-adjusted mean in the WMS-IV LMII of less than or equal to 15 for a subject of age ranging from 50 to 64 years, of less than or equal to 12 for a subject of age ranging from 65 to 69 years, of less than or equal to 11 for a subject of age ranging from 70 to 74 years, of less than or equal to 9 for a subject of age ranging from 75 to 79 years. 75. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising subcutaneously administering to the subject 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg), of an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3). 76. A method of delaying clinical decline in a subject having AD, suspected of having AD, or at risk for AD, comprising subcutaneously administering to the subject 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg), of an anti-Aβ protofibril antibody comprising three heavy chain Attorney Docket No.08061.0062-00304 complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3). 77. A method of reducing brain amyloid level in a subject having AD, suspected of having AD, or at risk for AD, comprising subcutaneously administering to the subject 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg), of an antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3). 78. A method of converting an amyloid positive subject to amyloid negative comprising subcutaneously administering to the subject 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg), of an antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3). 79. The method of any one of embodiments 75-78, wherein the antibody subcutaneously administered at 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg) reduces a biomarker of AD pathology and/or provides a lower systemic exposure (e.g., AUC) to the antibody than for a higher dose such as 720 mg administered subcutaneously. 80. The method of any one of embodiments 75-79, wherein the antibody subcutaneously administered at 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg) reduces a risk for developing ARIA relative to a higher dose of the antibody, such as 720 mg administered subcutaneously. 81. The method of any one of embodiments 75-80, wherein the anti-Aβ protofibril antibody is administered at a dose of 150 mg to 200 mg, 200 mg to 250 mg, 250 mg to 300 mg, 350 mg to 400 mg, 450 mg to 500 mg, or 550 mg to 600 mg. 82. The method of any one of embodiments 75-81, wherein the anti-Aβ protofibril antibody is administered subcutaneously at a dose of 500 mg. 83. The method of any one of embodiments 75-82, wherein the dose is administered in two parts, e.g., consecutively. Attorney Docket No.08061.0062-00304 84. The method of any one of embodiments 75-83, wherein the anti-Aβ protofibril antibody is administered once weekly. 85. The method of any one of embodiments 75-83, wherein the anti-Aβ protofibril antibody is administered once biweekly. 86. The method of any one of embodiments 75-83, wherein the anti-Aβ protofibril antibody is administered once monthly. 87. The method of any one of embodiments 75-86, wherein the anti-Aβ protofibril antibody is administered at an initiation dose for a first time period, e.g., according to an initiation dosing regimen, and administered at a maintenance dose for a second time period, e.g., according to a maintenance dosing regimen. 88. The method of embodiment 87, wherein the initiation dose is 500 mg. 89. The method of embodiment 87 or embodiment 88, wherein the initiation dose is greater than the maintenance dose. 90. The method of any one of embodiments 87-89, wherein the maintenance dose is 360 mg. 91. The method of any one of embodiments 87-90, wherein the maintenance dose is 250 mg. 92. The method of any one of embodiments 87-91, wherein the initiation dose is administered weekly. 93. The method of any one of embodiments 87-92, wherein the maintenance dose is administered weekly. 94. The method of any one of embodiments 87-92, wherein the maintenance dose is administered biweekly. 95. The method of any one of embodiments 87-94, wherein the first time period is at least about 6 months, about 12 months, about 18 months, about 24 months, or about 30 months. 96. The method of embodiment 95, wherein the first time period is at least 18 months. 97. The method of embodiment 95 or embodiment 96, wherein the first time period is at least 24 months. 98. The method of any one of embodiments 87-97, wherein the first time period lasts until the subject is amyloid negative. 99. The method of any one of embodiments 87-98, wherein the anti-protofibril antibody (e.g., BAN2401) is subcutaneously administered at an initiation dose of 500 mg weekly for at least 18 months, and then subcutaneously administered at a maintenance dose of 250 mg weekly for the second period of time. Attorney Docket No.08061.0062-00304 100. The method of any one of embodiments 87-98, wherein the anti-protofibril antibody (e.g., BAN2401) is subcutaneously administered at an initiation dose of 500 mg weekly for at least 18 months, and then subcutaneously administered at a maintenance dose of 360 mg biweekly for the second period of time. 101. The method of any one of embodiments 87-100, wherein the second time period begins when one or more biomarkers in the subject indicate a reduction in or slowing of AD progression. 102. The method of any one of embodiments 87-101, wherein the second time period is at least about 6 months, about 12 months, about 18 months, about 24 months, about 36 months, about 42 months, about 48 months, about 54 months, about 60 months, or for the lifetime of the subject. 103. The method of any one of embodiments 87-102, wherein the maintenance dose is subcutaneously administered with an autoinjector (AI). 104. The method of any one of embodiments 75-103, wherein the anti-Aβ protofibril antibody is administered subcutaneously to the subject after intravenous administration of the antibody. 105. The method of any one of embodiments 75-103, wherein the anti-Aβ protofibril antibody is administered subcutaneously to the subject prior to intravenous administration of the antibody. 106. The method of embodiment 104 or embodiment 105, wherein the intravenous infusion is 10 mg/kg relative to the weight of the subject, administered biweekly. 107. The method according to any one of embodiments 75-106, wherein the anti-Aβ protofibril antibody is comprised in a pharmaceutical composition in the form of a pre-filled syringe. 108. The method according to any one of embodiments 75-106, wherein the anti-Aβ protofibril antibody is comprised in a pharmaceutical composition in an autoinjector. 109. The method according to any one of embodiments 75-108, wherein the anti-Aβ protofibril antibody comprising a heavy chain complementarity variable region comprising an amino acid sequence of SEQ ID NO: 1, and a light chain variable region comprising an amino acid sequence of SEQ ID NO: 2. 110. The method according to any one of embodiments 75-108, wherein the anti-Aβ protofibril antibody is BAN2401 (lecanemab). 111. The method of any one of embodiments 75-110, wherein the subject shows a change in a measurement of one or more biomarkers associated with AD pathology prior to treatment. 112. The method of embodiment 111, wherein the change in the measurement is selected from: a. increased amyloid in the brain, e.g., as measured by amyloid PET (e.g., a centiloid measure of about 20-40, e.g., a centiloid measure of about 20-32), Attorney Docket No.08061.0062-00304 b. increased tau in the brain, e.g., as measured by positron emission tomography (PET), c. decreased cerebrospinal fluid levels of ratio of Aβ1-42/1-40 and/or increased total tau, p- tau (e.g., p-tau181, p-tau217, and/or p-tau231), the ratio of p-tau181/np-tau181, and/or the ratio of p- tau217/np-tau217, neurogranin, and/or neurofilament light chain (NfL), and d. decreased blood serum or plasma levels of a ratio of Aβ1-42/1-40 and/or increased total tau, phosphorylated tau (P-tau) isoforms (e.g., P-tau181, P-tau217, and/or P-tau231), ratio of p- tau181/np-tau181, the ratio of p-tau217/np-tau217, glial fibrillary acidic protein (GFAP), and/or neurofilament light chain (NfL). 113. The method of any one of embodiments 75-112, wherein the subject is amyloid-positive prior to administration, e.g., as indicated by a PET assessment, a CSF assessment of Aβ(1-42), MRI, retinal amyloid accumulation, and/or a blood biomarker assessment (e.g. a plasma Aβ1-42/1-40 ratio, plasma p-tau181, plasma p-tau217, plasma p-tau 231 level, the ratio of p-tau181/np-tau181, and/or the ratio of p-tau217/np-tau217). 114. The method according to any one of embodiments 75-113, wherein the subject is ApoE4- positive. 115. The method of any one of embodiments 75-114, wherein the subject is monitored for development of ARIA. 116. The method any one of embodiments 75-115, wherein the subject is 65 to 80 years old. 117. The method any one of embodiments 75-115, wherein the subject is 55 to 64 years old and has at least one risk factor chosen from: (i) a first degree relative diagnosed with dementia onset before age 75; (ii) at least one apolipoprotein E4 variant (APOE4) allele; and (iii) elevated brain amyloid according to PET or cerebrospinal fluid (CSF) testing prior to said administration. 118. The method of any one of embodiments 75-117, wherein the subject has Alzheimer’s disease. 119. The method of any one of embodiments 75-118, wherein the subject has early Alzheimer’s disease. 120. The method of any one of embodiments 75-119, wherein the subject has been diagnosed with a. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood and/or has been diagnosed as having mild Alzheimer’s disease dementia; Attorney Docket No.08061.0062-00304 b. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by National Institute of Aging – Alzheimer’s Association (NIA-AA) core clinical criteria; c. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by a CDR global score of 0.5 and a Memory Box score of 0.5 or greater before treatment; d. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by a history of subjective memory decline with gradual onset and slow progression over the last 1 year before treatment, e.g., as corroborated by an informant; e. mild Alzheimer’s disease dementia by the NIA-AA core clinical criteria for probable Alzheimer’s disease dementia; or f. mild Alzheimer’s disease dementia by a CDR score of 0.5 to 1.0 and a Memory Box score of 0.5 or greater before treatment. 121. The method of any one of embodiments 75-117, wherein the subject is suspected of having AD. 122. The method of any one of embodiments 75-117, wherein the subject is a subject at risk for developing AD. 123. The method of embodiment 122, wherein the subject at risk for developing AD has pre-AD. 124. The method of embodiment 123 or embodiment 124, wherein the subject does not have cognitive impairment. 125. The method of any one of embodiments 122-124, wherein the subject has a Global Clinical Dementia Rating (CDR) score of 0 at prior to said administration. 126. The method of any one of embodiments 122-125, wherein the subject has a Mini-Mental State Examination (MMSE) score greater than or equal to 27, with educational adjustments, prior to said administration. 127. The method of any one of embodiments 122-126, wherein the subject has a Wechsler Memory Scale-Revised Logical Memory subscale II (WMS-R LM II) score prior to said administration of at least one standard deviation below age-adjusted mean in the WMS-IV LMII of less than or equal to 15 for a subject of age ranging from 50 to 64 years, of less than or equal to 12 for a subject of age ranging from 65 to 69 years, of less than or equal to 11 for a subject of age ranging from 70 to 74 years, of less than or equal to 9 for a subject of age ranging from 75 to 79 years, and of less than or equal to 7 for a subject of age ranging from 80 to 90 years. 128. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) Attorney Docket No.08061.0062-00304 comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the antibody biweekly at an initiation dose of 10 mg/kg relative to the weight of the subject; and subcutaneously administering, e.g., after 18 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose, of 250 mg, 360 mg, or 500 mg. 129. A method of delaying clinical decline in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the antibody biweekly at an initiation dose of 10 mg/kg relative to the weight of the subject; and subcutaneously administering, e.g., after 18 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg, 360 mg, or 500 mg. 130. A method of reducing brain amyloid level in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg), of an antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the antibody biweekly at an initiation dose of 10 mg/kg relative to the weight of the subject; and subcutaneously administering, e.g., after 18 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg, 360 mg, or 500 mg. 131. A method of converting an amyloid positive subject to amyloid negative comprising administering to the subject an antibody comprising three heavy chain complementarity determining Attorney Docket No.08061.0062-00304 regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3) , according to a dosage regimen comprising: intravenously administering the antibody biweekly at an initiation dose of 10 mg/kg relative to the weight of the subject; and subcutaneously administering, e.g., after 18 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg, 360 mg, or 500 mg. 132. The method of any one of embodiments 128-131, wherein the maintenance dose is 500 mg. 133. The method of any one of embodiments 128-131, wherein the maintenance dose is 360 mg. 134. The method of any one of embodiments 128-131, wherein the maintenance dose is 250 mg. 135. The method of any one of embodiments 128-134, wherein the initiation dose of the antibody is administered intravenously for at least 6 months, at least 12 months, at least 18 months, or at least 24 months. 136. The method of any one of embodiments 128-135, wherein the initiation dose of the antibody is administered intravenously for at least 18 months. 137. The method of any one of embodiments 128-136, wherein the initiation dose of the antibody is administered intravenously for at least 24 months. 138. The method of any one of embodiments 128-137, wherein the maintenance dose of the antibody is administered weekly. 139. The method of any one of embodiments 128-137, wherein the maintenance dose of the antibody is administered biweekly. 140. The method of any one of embodiments 128-139, wherein the maintenance dose of the antibody is administered using a vial-syringe. 141. The method of any one of embodiments 128-139, wherein the maintenance dose of the antibody is administered using an AI. 142. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and Attorney Docket No.08061.0062-00304 LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: subcutaneously administering the antibody weekly at an initiation dose of 500 mg; and subcutaneously administering, e.g., after 18 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg. 143. A method of delaying clinical decline in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: subcutaneously administering the antibody weekly at an initiation dose of 500 mg; and subcutaneously administering, e.g., after 18 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg. 144. A method of reducing brain amyloid level in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg), of an antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: subcutaneously administering the antibody weekly at an initiation dose of 500 mg; and subcutaneously administering, e.g., after 18 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg. 145. A method of converting an amyloid positive subject to amyloid negative comprising administering to the subject an antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3) , according to a dosage regimen comprising: Attorney Docket No.08061.0062-00304 subcutaneously administering the antibody weekly at an initiation dose of 500 mg; and subcutaneously administering, e.g., after 18 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg. 146. The method of any one of embodiments 142-145, wherein the initiation dose of the antibody is administered subcutaneously for at least 6 months, at least 12 months, at least 18 months, or at least 24 months. 147. The method of any one of embodiments 142-146, wherein the initiation dose of the antibody is administered subcutaneously for at least 18 months. 148. The method of any one of embodiments 142-147, wherein the initiation dose of the antibody is administered subcutaneously for at least 24 months. 149. The method of any one of embodiments 142-148, wherein the initiation dose of the antibody is administered using a vial-syringe. 150. The method of any one of embodiments 142-148, wherein the initiation dose of the antibody is administered using an AI. 151. The method of any one of embodiments 142-150, wherein the maintenance dose of the antibody is administered weekly. 152. The method of any one of embodiments 142-150, wherein the maintenance dose of the antibody is administered biweekly. 153. The method of any one of embodiments 142-152, wherein the maintenance dose of the antibody is administered using a vial-syringe. 154. The method of any one of embodiments 142-152, wherein the maintenance dose of the antibody is administered using an AI. 155. The method according to any one of embodiments 128-154, wherein the anti-Aβ protofibril antibody comprising a heavy chain complementarity variable region comprising an amino acid sequence of SEQ ID NO: 1, and a light chain variable region comprising an amino acid sequence of SEQ ID NO: 2. 156. The method according to any one of embodiments 128-155, wherein the anti-Aβ protofibril antibody is BAN2401 (lecanemab). 157. The method of any one of embodiments 128-156, wherein the subject shows a change in a measurement of one or more biomarkers associated with AD pathology prior to treatment. 158. The method of embodiment 157, wherein the change in the measurement is selected from: Attorney Docket No.08061.0062-00304 a. increased amyloid in the brain, e.g., as measured by amyloid PET (e.g., a centiloid measure of about 20-40, e.g., a centiloid measure of about 20-32), b. increased tau in the brain, e.g., as measured by positron emission tomography (PET), c. decreased cerebrospinal fluid levels of a ratio of Aβ1-42/1-40, and/or increased total tau, p- tau (e.g, p-tau181, p-tau217, and/or p-tau231), ratio of p-tau181/np-tau181, ratio of p-tau217/np- tau217, neurogranin, and/or neurofilament light chain (NfL), and d. decreased blood serum or plasma levels of a ratio of Aβ1-42/1-40 and/or increased total tau, phosphorylated tau (P-tau) isoforms (e.g., P-tau181, P-tau217, and/or P-tau231, ratio of p- tau181/np-tau181, ratio of p-tau217/np-tau217, glial fibrillary acidic protein (GFAP), and/or neurofilament light chain (NfL). 159. The method of any one of embodiments 128-158 wherein the subject is amyloid-positive prior to administration, e.g., as indicated by a PET assessment, a CSF assessment of Aβ(1-42), MRI, retinal amyloid accumulation. 160. The method according to any one of embodiments 128-159, wherein the subject is ApoE4- positive. 161. The method of any one of embodiments 128-160, wherein the subject is monitored for development of ARIA. 162. The method any one of embodiments 128-161, wherein the subject is 65 to 80 years old. 163. The method any one of embodiments 128-161, wherein the subject is 55 to 64 years old and has at least one risk factor chosen from: (i) a first degree relative diagnosed with dementia onset before age 75; (ii) at least one apolipoprotein E4 variant (APOE4) allele; and (iii) elevated brain amyloid according to PET or cerebrospinal fluid (CSF) testing prior to said administration. 164. The method of any one of embodiments 128-163, wherein the subject has Alzheimer’s disease. 165. The method of any one of embodiments 128-164, wherein the subject has early Alzheimer’s disease. 166. The method of any one of embodiments 128-165, wherein the subject has been diagnosed with a. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood and/or has been diagnosed as having mild Alzheimer’s disease dementia; Attorney Docket No.08061.0062-00304 b. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by National Institute of Aging – Alzheimer’s Association (NIA-AA) core clinical criteria; c. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by a CDR global score of 0.5 and a Memory Box score of 0.5 or greater before treatment; d. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by a history of subjective memory decline with gradual onset and slow progression over the last 1 year before treatment, e.g., as corroborated by an informant; e. mild Alzheimer’s disease dementia by the NIA-AA core clinical criteria for probable Alzheimer’s disease dementia; or f. mild Alzheimer’s disease dementia by a CDR score of 0.5 to 1.0 and a Memory Box score of 0.5 or greater before treatment. 167. The method of any one of embodiments 128-166, wherein the subject is suspected of having AD. 168. The method of any one of embodiments 128-163, wherein the subject is a subject at risk for developing AD. 169. The method of embodiment 168, wherein the subject at risk for developing AD has pre-AD. 170. The method of any one of embodiments 168 or embodiment 169, wherein the subject does not have cognitive impairment. 171. The method of any one of embodiments 168-170, wherein the subject has a Global Clinical Dementia Rating (CDR) score of 0 at prior to said administration. 172. The method of any one of embodiments 168-171, wherein the subject has a Mini-Mental State Examination (MMSE) score greater than or equal to 27, with educational adjustments, prior to said administration. 173. The method of any one of embodiments 168-172, wherein the subject has a Wechsler Memory Scale-Revised Logical Memory subscale II (WMS-R LM II) score prior to said administration of at least one standard deviation below age-adjusted mean in the WMS-IV LMII of less than or equal to 15 for a subject of age ranging from 50 to 64 years, of less than or equal to 12 for a subject of age ranging from 65 to 69 years, of less than or equal to 11 for a subject of age ranging from 70 to 74 years, of less than or equal to 9 for a subject of age ranging from 75 to 79 years, and of less than or equal to 7 for a subject of age ranging from 80 to 90 years. 174. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising Attorney Docket No.08061.0062-00304 amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the antibody biweekly at an initiation dose of 10 mg/kg relative to the weight of the subject; and intravenously administering, e.g., after 18 or 24 months at the initiation dose, the antibody monthly at a dose of 10 mg/kg relative to the weight of the subject. 175. A method of delaying clinical decline in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the antibody biweekly at an initiation dose of 10 mg/kg relative to the weight of the subject; and intravenously administering, e.g., after 18 or 24 months at the initiation dose, the antibody monthly at a dose of 10 mg/kg relative to the weight of the subject. 176. A method of reducing brain amyloid level in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg), of an antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the antibody biweekly at an initiation dose of 10 mg/kg relative to the weight of the subject; and intravenously administering, e.g., after 18 or 24 months at the initiation dose, the antibody monthly at a dose of 10 mg/kg relative to the weight of the subject. 177. A method of converting an amyloid positive subject to amyloid negative comprising administering to the subject an antibody comprising three heavy chain complementarity determining Attorney Docket No.08061.0062-00304 regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3) , according to a dosage regimen comprising: intravenously administering the antibody biweekly at an initiation dose of 10 mg/kg relative to the weight of the subject; and intravenously administering, e.g., after 18 months at the initiation dose, the antibody monthly at a dose of 10 mg/kg relative to the weight of the subject. 178. A method of treating a subject having early AD, suspected of having early AD, or at risk for early AD, and who has received a first anti-Aβ antibody, comprising: administering to the subject a second anti-Aβ antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the second antibody biweekly or monthly at a maintenance dose of 10 mg/kg relative to the weight of the subject; or subcutaneously administering the second antibody weekly or biweekly at a maintenance dose, of 250 mg, 360 mg, or 500 mg. 179. A method of delaying clinical decline in a subject who has received a first anti-Aβ antibody, comprising: administering to the subject a second anti-Aβ antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the second antibody biweekly or monthly at a maintenance dose of 10 mg/kg relative to the weight of the subject; or subcutaneously administering the second antibody weekly or biweekly at a maintenance dose of 250 mg, 360 mg, or 500 mg. Attorney Docket No.08061.0062-00304 180. A method of reducing a brain amyloid level in a subject in a subject who has received a first anti-Aβ antibody, comprising: administering to the subject 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg), of a second anti-Aβ antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the second antibody biweekly or monthly at a maintenance dose of 10 mg/kg relative to the weight of the subject; or subcutaneously administering the second antibody weekly or biweekly at a maintenance dose of 250 mg, 360 mg, or 500 mg. 181. A method of maintaining amyloid levels in a subject who has received a first anti-Aβ antibody, comprising: administering to the subject a second anti-Aβ antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3) , according to a dosage regimen comprising: intravenously administering the second antibody biweekly or monthly at a maintenance dose of 10 mg/kg relative to the weight of the subject; or subcutaneously administering the second antibody weekly or biweekly at a maintenance dose of 250 mg, 360 mg, or 500 mg. 182. A method of treating a subject having early AD, suspected of having early AD, or at risk for early AD, comprising: administering to the subject a first anti-Aβ antibody, administering to the subject a second anti-Aβ antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising Attorney Docket No.08061.0062-00304 amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the second antibody biweekly or monthly at a maintenance dose of 10 mg/kg relative to the weight of the subject; or subcutaneously administering the second antibody weekly or biweekly at a maintenance dose, of 250 mg, 360 mg, or 500 mg. 183. The method of any one of embodiments 178-182, wherein the subcutaneously administered maintenance dose is 500 mg. 184. The method of any one of embodiments 178-182, wherein the subcutaneously administered maintenance dose is 360 mg. 185. The method of any one of embodiments 178-182, wherein the subcutaneously administered maintenance dose is 250 mg. 186. The method of any one of embodiments 178-185, wherein the subcutaneously administered maintenance dose of the antibody is administered using a vial-syringe. 187. The method of any one of embodiments 178-185, wherein the subcutaneously administered maintenance dose of the antibody is administered using an AI. 188. The method of any one of embodiments 178-187, wherein the first anti-Aβ antibody is selected from aducanumab, bapineuzumab, crenezumab, donanemab, gantenerumab, lecanemab, or solanezumab. 189. The method of embodiment 188, wherein the first anti-Aβ antibody is donanemab. 190. A method of treating a subject having early AD, suspected of having early AD, or at risk for early AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: subcutaneously administering the antibody weekly at an initiation dose of 500 mg; and subcutaneously administering, e.g., after 18 or 24 months at the initiation dose, the antibody weekly at a dose of 360 mg. 191. A method of treating a subject having early AD, suspected of having early AD, or at risk for early AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three Attorney Docket No.08061.0062-00304 heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the antibody biweekly at a first initiation dose of 10 mg/kg relative to the weight of the subject; subcutaneously administering the antibody weekly at a second initiation dose of 720 or 500 mg; and subcutaneously administering, e.g., after 18 or 24 months of treatment on the initiation doses, the antibody weekly at a dose of 360 or 250 mg. BRIEF DESCRIPTION OF DRAWINGS Figure 1 shows the results for CDR-SB, ADAS-cog14, and ADCS MCI-ADL in Study 301. Figure 2 shows the adjusted mean change from baseline in CDR-SB in Study 301. Figure 3 shows the adjusted mean change from baseline in ADAS-Cog14 in Study 301. Figure 4 shows the adjusted mean change from baseline in ADCS MCI-ADL in Study 301. Figure 5 shows the reduction in brain amyloid beta plaque (adjusted mean change from baseline in amyloid beta PET centiloids) in Study 301. Figure 6 shows the health-related quality of life measures EQ-5D-5L (Health Today Subject). Figure 7 shows the health-related quality of life measures QOL-AD (Total Score Subject). Figure 8 shows the health-related quality of life measures QOL-AD (Subject by Proxy). Figure 9 shows the health-related quality of life measures Zarit Burden Interview – Study Partner Burden (Total Score). Figure 10 shows the time to worsening of global CDR scores. Figure 11 shows the slope analysis using CDR-SB: observed data and extrapolation to 2 Years. Figure 12 shows the change in plasma GFAP by treatment. Attorney Docket No.08061.0062-00304 Figure 13 shows ARIA rates and antithrombotic use in the Clarity AD double-blind core period. Figure 14 shows ARIA rates and antithrombotic use by genotype in the Clarity AD double-blind core period. Figure 15 shows ARIA rates and antithrombotic use in Clarity AD Core and OLE. Figure 16 shows ARIA rates and antithrombotic use by genotype in Clarity AD Core and OLE. Figure 17 shows expected ARIA-E rates for autoinjector and IV. Figure 18 shows average steady-state concentrations for routes of administration. Figure 19 shows baseline clinical characteristics of Study 301. Figure 20 shows results for primary and key secondary endpoints from Study 301. Figure 21 shows the overall safety profile from Study 301. Figure 22 shows ARIA and infusion-related reaction differences from placebo in Study 301. Figure 23 shows infusion-related reaction grades and timing in treatment in Study 301. Figure 24 shows ARIA-E events in 897 subjects who received a placebo and 898 subjects who received leacanemab. Figure 25 shows that ~90% of ARIA-E cases occurred after ≤ 6 months of treatment, and resolved within 4 months of detection. Figure 25A shows the probability of ARIA-E occurrence from 0-76 weeks. Figure 25B shows the probability of ARIA-E occurrence from 0-120 weeks. Figure 26 shows that isolated ARIA-H (without ARIA-E) occurred at a similar rate between lecanemab and placebo in Study 301. Figure 27 shows that most ARIA-H events were microhemorrhages and superficial siderosis in conjunction with ARIA-E in Study 301. Figure 28 shows that rates of ARIA were not increased with concurrent antiplatelet or anticoagulant use relative to lecanemab alone. Figure 29 shows event rates of ARIA, ARIA-E and ARIA-H based on APOE4 carrier status. Figure 30 shows a summary of ARIA case by number of microhemorrhages at baseline, by APOE4 status. Attorney Docket No.08061.0062-00304 Figure 31 shows a concentration-time profile of lecanemab following single intravenous (10 mg/kg; n=30) and subcutaneous (700 mg; n=29) doses. Figure 32 shows a concentration-time profile of lecanemab following a single subcutaneous (700 mg) dose in Japanese (n=5) versus non Japanese subjects (n=24) Figure 33 shows the mean (SD) serum concentration-time curves of lecanemab, presented on a linear and semi-logarithmic scale, comparing subcutaneous administration from a vial/syringe and via an AI device. Figure 34 shows boxplots for C_max of lecanemab in serum after 720 mg subcutaneous lecanemab injection with vial and syringe (Vial/Syringe) or 720 mg subcutaneous lecanemab injection with an autoinjector (AI) (PK analysis set). Figure 35 shows boxplots for AUC(_0-inf) of lecanemab in serum after 720 mg subcutaneous lecanemab injection with vial and syringe (Vial/Syringe) or 720 mg subcutaneous lecanemab injection with an autoinjector (AI) (PK analysis set). Figure 36 shows boxplots for AUC(0-t) of lecanemab in serum after 720 mg subcutaneous lecanemab injection with vial and syringe (Vial/Syringe) or 720 mg subcutaneous lecanemab injection with an autoinjector (AI) (PK analysis set). Figure 37 shows an overview of the study design for Study 301, including the Core Study, Extension Study, and Subcutaneous Substudies. Figure 38 shows the effect of body weight on model predicted lecanemab exposure (and their ratio) following fixed 720 mg weekly SC (vial/syringe) and 10 mg/kg biweekly IV dosing. Figure 39 shows a comparison of average steady-state concentration following 10 mg/kg biweekly IV (Study 301 Core and OLE) or 720 mg SC AI Weekly (Study 301 OLE AI Substudy). Figure 40 shows simulated lecanemab average steady-state concentrations (C_ave,ss) for SC 500 mg QW administered using 2 AI devices and model-predicted (observed) C_ave,ss for IV LEC10- BW in Study 301 core and OLE phase. Figure 41 shows a model projected median (90% prediction interval) amyloid PET following either 10 mg/kg IV biweekly or 500 mg SC AI weekly lecanemab. Figure 42 shows a model projected mean (90% prediction interval) change in CDR-SB following either 10 mg/kg IV biweekly or 500 mg SC AI weekly lecanemab. Figure 43 shows a projected change in amyloid PET for subjects receiving 10 mg/kg IV for 18 or 24 Months, followed by 360 mg SC AI weekly compared to placebo or continuous 10 mg/kg IV Lecanemab. Attorney Docket No.08061.0062-00304 Figure 44 shows a projected change in CDR-SB for subjects receiving 10 mg/kg IV for 18 or 24 months, followed by 360 mg SC AI weekly compared to placebo or continuous 10 mg/kg IV lecanemab. Figure 45 shows simulated amyloid PET profiles for IV LEC10-BW dosing over 4 years, compared to initiation of SC 360 mg QW (1x AI Device) or LEC10-M, for a maintenance dose at 18 and 24 months in subjects with baseline amyloid PET ≥60 and <60 Centiloids. AI = autoinjector, BW = biweekly, CL = Centiloids, IV = intravenous, PET = positron emission tomography, QW = weekly, Q4W = every 4 weeks. Figure 46 shows simulated CDR-SB profiles for IV LEC10-BW dosing for 4 years, compared to initiation of SC 360 mg QW (1x AI Device) or LEC10-M, for a maintenance dose at 18 and 24 months in subjects with baseline amyloid PET ≥60 and <60 Centiloids. AI = autoinjector, BW = biweekly, CL = Centiloids, IV = intravenous, PET = positron emission tomography, QW = weekly, Q4W = every 4 weeks. Figure 47 shows model-predicted plasma Aβ42/40 ratio and p-tau181 after various dosing regimens. AI = autoinjector, BW = biweekly, CI = Confidence Intervals, QW = weekly, Q4W = every 4 weeks. Solid line and shaded area show predicted median and 95% CI, respectively. P-tau181 = human tau protein phosphorylated at threonine in position 181. Figure 48 shows SC exposures in healthy volunteers (Study 005) and Study 301 OLE AI device substudy (AD subjects) compared to IV LEC10-BW. AD = Alzheimer’s disease; HV = healthy volunteers; IV = intravenous; n=168 with both IV and AD device. Figure 49 shows SC exposures following 360 mg QW AI maintenance doses are within the range of LEC10-BW. Figure 50 shows a Kaplan-Meier (KM) plot of actual duration for time to event. DETAILED DESCRIPTION The “amyloid hypothesis” proposes that amyloid β (Aβ) peptides play a central role in the pathogenesis of AD. Specifically, it is hypothesized that neurodegeneration in AD may be caused by deposition of Aβ plaques in brain tissue due to an imbalance between Aβ production and Aβ clearance, leading to formation of neurofibrillary tangles containing tau protein. Aβ peptides generally exist in a dynamic continuum of conformational states such that species tend to progress from monomeric Aβ, to soluble Aβ assemblies that include a range of low molecular weight oligomers to higher molecular weight protofibrils, and finally to insoluble fibrils (plaques). Targeting these soluble and insoluble Aβ tangles and plaques may provide therapeutic benefit. Attorney Docket No.08061.0062-00304 A number of immunotherapies have been developed with the intent to reduce the amount of insoluble Aβ fibrils deposited in the brain. However, a simple correlation between the quantity and progressive accumulation of insoluble amyloid plaques and the clinical course of AD has not been determined. While therapeutic strategies continue to focus on removal of insoluble amyloid plaques, an additional approach to therapy may include reducing the toxic Aβ aggregates, such as protofibrils, that may contribute to the neuronal degeneration characteristic of AD. (See, e.g., Dodort, J.-C. and May, P., “Overview on rodent models of Alzheimer’s disease.” Curr. Protocols Neurosci.2005; 9.22- 1-9.22-6; Englund, H. et al., “Sensitive ELISA detection of amyloid-β protofibrils in biological samples.” J. Neurochem.2007; 103:334-45; and Gotz, J. et al., “Transgenic animal models of Alzheimer’s disease and related disorders: histopathology, behavior and therapy.” Mol. Psychiat. 2004; 9:664-83.) In various embodiments, anti-Aβ protofibril antibodies, such as BAN2401 and other anti- Aβ protofibril antibodies, may be used to treat AD, e.g., by slowing AD progression in subjects, e.g., those at early stages of the disease when amyloid has been deposited in the brain but where the downstream neurodegenerative cascade thought to be triggered by the amyloid deposition is still relatively early in its course (i.e., limited brain tissue loss has been produced and associated clinical deficits are at a minimum). In various embodiments, methods are disclosed herein for selecting a patient suitable for treatment with an anti-Aβ protofibril antibody, such as BAN2401, wherein the patient is at lower risk of developing ARIA, e.g., wherein the patient has not had a brain hemorrhage event, e.g., a microhemorrhage or intracerebral hemorrhage, and/or wherein the patient is not an ApoE4 carrier, prior to treatment. In various embodiments, methods are disclosed herein for selecting a patient suitable for treatment with an anti-Aβ protofibril antibody, such as BAN2401, wherein the patient is at lower risk of developing ARIA, e.g., wherein the patient has not exhibited a change, e.g., a decrease, in brain white matter at the time of treatment. In various embodiments, methods are disclosed herein for selecting a patient suitable for treatment with an anti-Aβ protofibril antibody, such as BAN2401, wherein the patient is at lower risk of developing ARIA, e.g., wherein the patient is not on an anticoagulant at the time of treatment, not on a thrombolytic agent, and/or wherein the patient is not an ApoE4 carrier. In various embodiments, methods are disclosed herein for treating a patient with Alzheimer’s disease or suspected of having Alzheimer’s disease, wherein the patient is at a lower risk of developing ARIA based on brain imaging. In some embodiments, a patient that does not have a brain hemorrhage, e.g., a microhemorrhage or intracerebral hemorrhage, on baseline imaging is administered an anti-amyloid β (Aβ) protofibril antibody (e.g., BAN2401). In some embodiments, a patient that has had a brain hemorrhage, e.g., a microhemorrhage or intracerebral hemorrhage, on Attorney Docket No.08061.0062-00304 baseline imaging is not administered an anti-amyloid β (Aβ) protofibril antibody (e.g., BAN2401). In some embodiments, a patient that does not exhibit a change, e.g., a decrease, in brain white matter as measured by brain imaging prior to treatment is administered an anti-amyloid β (Aβ) protofibril antibody (e.g., BAN2401). In some embodiments, a patient that exhibits a change, e.g., a decrease, in brain white matter as measured by brain imaging is not administered an anti-amyloid β (Aβ) protofibril antibody (e.g., BAN2401). In various embodiments, methods are disclosed herein for selecting and treating a patient with Alzheimer’s disease or suspected of having Alzheimer’s disease, wherein the patient is at a lower risk of developing ARIA, e.g., based on the use of anticoagulants or thrombolytic agents. In some embodiments, a patient receiving aspirin is administered a therapeutically effective dose of an anti- amyloid β (Aβ) protofibril antibody (e.g., BAN2401). In some embodiments, a patient receiving an antiplatelet medication is administered a therapeutically effective dose of an anti-amyloid β (Aβ) protofibril antibody (e.g., BAN2401). In some embodiments, a patient receiving a thrombolytic and/or anticoagulant agent is administered a therapeutically effective dose of an anti-amyloid β (Aβ) protofibril antibody (e.g., BAN2401). In some embodiments, a patient receiving an anticoagulant is not selected for treatment with an anti-amyloid β (Aβ) protofibril antibody (e.g., BAN2401). In some embodiments, a patient receiving a thrombolytic agent is not selected for treatment with an anti- amyloid β (Aβ) protofibril antibody (e.g., BAN2401). In various embodiments, methods are disclosed herein for treating a patient with Alzheimer’s disease or suspected of having Alzheimer’s disease wherein the patient is at an increased risk of an ARIA event or brain hemorrhage, e.g., a microhemorrhage, a intracerebral hemorrhage, wherein the patient is administered an anti-amyloid β (Aβ) protofibril antibody (e.g., BAN2401) and is further administered a steroid. In some embodiments, a patient receiving an anti-amyloid β (Aβ) protofibril antibody and has a severe ARIA event is administered a steroid. In some embodiments, additional patient demographics, such as age and if the subject is a carrier of the apolipoprotein E ε4 gene allele, may be used to select a patient for treatment in combination with baseline status of brain hemorrhage, e.g., presence or absence of microhemorrhage or intracerebral hemorrhage, baseline status of brain white matter, and/or treatment with an anticoagulant or thrombolytic agent, and/or additional biomarkers indicating amyloid positivity (e.g. West et al, Mol Neurodegen (2021) 16-30, Jansen et al, JAMA (2015) 1924-1938, Ossenkoppele et al, JAMA (2015) 1939-1950). In some embodiments, one or more additional biomarkers, e.g., one or more blood biomarkers (such as the ratio of Aβ 42 to Aβ 40 and/or a p-tau181) may be used to select a patient, e.g., in conjunction with brain measurements such as an amyloid or tau PET measurement. In some Attorney Docket No.08061.0062-00304 embodiments, biomarkers associated with AD pathology include (but are not limited to) one or more of: ^ amyloid in the brain (e.g., as measured by amyloid positron emission tomography (PET); ^ tau in the brain (e.g., as measured by tau PET; ^ cerebrospinal fluid (CSF) biomarkers, e.g., CSF levels of Aβ42, Aβ40, Aβ42/Aβ40 ratio, total tau, p-tau (e.g., p-tau181, p-tau217, p-tau231), p-tau181/np-tau181 ratio, p-tau217/np-tau217 ratio; neurogranin; neurofilament light chain (NfL), and/or glial fibrillary acidic protein (GFAP); ^ blood biomarkers, e.g., plasma and/or serum levels of Aβ42, Aβ40, Aβ42/Aβ40 ratio, total tau, p-tau (e.g., p-tau181, p-tau217, p-tau231), p-tau181/np-tau181 ratio, p-tau217/np-tau217 ratio; neurogranin; neurofilament light chain (NfL), and/or glial fibrillary acidic protein (GFAP); ^ biomarkers in other bodily fluids (e.g., urine, saliva, tears, sweat, etc.); ^ genetic biomarkers (e.g., ApoE4, PSEN1, and/or PSEN2); ^ abnormalities in eye and/or retinal vasculature (e.g., as measured by optical coherence tomography (OCT) or optical coherence tomography angiography (OCTA); and/or abnormalities in brain structure, function, and/or vasculature (e.g., as measured by magnetic resonance imaging (MRI), electroencephalograms (EEG), and/or single-photo emission computed tomography (SPECT). In some embodiments, an age and/or apolipoprotein E ε4 gene allele normalized measurement of tau PET and/or the at least one additional biomarker from a subject is used to evaluate whether a sample (e.g., a plasma sample) from a subject indicates that the subject is suitable for treatment with a protofibril antibody such as BAN2401 (e.g., if the subject is amyloid positive) and/or to monitor treatment. For example, in some embodiments, a patient who is a carrier of an apolipoprotein E ε4 gene allele may be considered amyloid positive at a lower level of a biomarker than needed to indicate amyloid positivity in a subject who is not a carrier. In some embodiments, a patient who is a carrier of an apolipoprotein E ε4 gene allele may be at a higher risk of developing ARIA in response to a treatment with an anti-amyloid β (Aβ) protofibril antibody (e.g., BAN2401), than a subject who is not a carrier and, e.g., may be cautioned by a doctor of increased risk, monitored for ARIA, and/or advised not to take an anti-amyloid β (Aβ) protofibril antibody (e.g., BAN2401). Likewise, in another example, an older subject may be considered amyloid positive at a lower biomarker level than the level required to indicate positivity in a younger subject. In some embodiments, biomarker level is used in a Receiver Operating Characteristic (ROC) analysis to predict amyloid positivity. In some embodiments, additional patient demographics, such as age and if the subject is a carrier of an apolipoprotein E ε4 gene allele, may be used with a biomarker level in an Attorney Docket No.08061.0062-00304 ROC analysis to predict amyloid positivity. In some embodiments, the prediction of amyloid positivity in a patient is used to determine the dosage or frequency of treatment. Cognitive and functional decline can be measured by techniques known in the art, including scoring methods such as CDR-SB, ADCOMS Composite Clinical Score, the Mini-Mental State Examination, ADAS-Cog, ADAS MCI-ADL, modified iADRS, Wechsler Memory Scale-IV Logical Memory (subscale) I (WMS-IV LMI), and Wechsler Memory Scale-IV Logical Memory (subscale) II (WMS-IV LMII). In some embodiments, the anti-Aβ protofibril antibody (e.g., BAN2401) is administered in a therapeutically effective amount to reduce or delay cognitive decline. In some embodiments, the anti-Aβ protofibril antibody (e.g., BAN2401) is administered as a therapeutically effective dose comprising an intravenous infusion of 10 mg/kg relative to the weight of the subject. In some embodiments, the anti-Aβ protofibril antibody (e.g., BAN2401) is administered as a therapeutically effective dose comprising a subcutaneous administration of 720 mg. In some embodiments, the method results in less cognitive decline as measured by ADCOMS compared to an untreated subject. In some embodiments, the method results in at least 24% less (e.g., at least 29% less) cognitive decline as measured by ADCOMS compared to an untreated subject. In some embodiments, the method results in less cognitive decline as measured by CDR-SB compared to an untreated subject. In some embodiments, the method results in at least 26% less (e.g., at least 27% less) cognitive decline as measured by CDR-SB compared to an untreated subject. In some embodiments, the method results in less cognitive decline as measured by ADAS-Cog14 compared to an untreated subject. In some embodiments, the method results in at least 26% less (e.g., at least 47% less) cognitive decline as measured by ADAS-Cog14 compared to an untreated subject. In some embodiments, the method results in less cognitive decline as measured by ADCS MCI-ADL compared to an untreated subject. In some embodiments, the method results in at least 37% less cognitive decline as measured by ADCS MCI-ADL compared to an untreated subject. In some embodiments, the method results in a reduced risk of progression to a subsequent stage of AD as measured by a CDR global score, e.g., a higher score on a subsequent evaluation indicating progression to the next stage of AD, e.g., an unchanged score indicating remaining in the same stage of AD. In some embodiments, the result is measured at least 6 months after administering a therapeutically effective amount of at least one anti-Aβ protofibril antibody. In some embodiments, the result is measured at least 12 months after administering a therapeutically effective amount of at least one anti-Aβ protofibril antibody. In some embodiments, the result is measured at least 13 months after administering a therapeutically effective amount of at least one anti-Aβ protofibril antibody. In some embodiments, the result is measured at least 18 months after administering a therapeutically effective amount of at least one anti-Aβ protofibril antibody. An anti-Aβ protofibril antibody, such as BAN2401, may be formulated in a pharmaceutical composition as disclosed in PCT/IB2021/000155 (WO2021/186245), which is Attorney Docket No.08061.0062-00304 incorporated herein by reference. In some embodiments, the composition comprises 80 mg/mL to 120 mg/mL BAN2401, 240 mM to 360 mM arginine, 0.03% w/v to 0.08% w/v polysorbate 80, and 30 mM to 70 mM citrate buffer. In some embodiments, the arginine is arginine, arginine hydrochloride, or a combination thereof. In some embodiments, the composition comprises a liquid dosage form comprising 100 mg/mL BAN2401, 50 mmol/L citrate, 350 mmol/L arginine, and 0.05% polysorbate 80. In some embodiments, the composition comprises 80 mg/mL to 240 mg/mL BAN2401, 140 mM to 260 mM arginine hydrochloride, 0.01% w/v to 0.1% w/v polysorbate 80, and 15 mM to 35 mM histidine buffer. In some embodiments, the composition comprises a liquid dosage form comprising 100 mg/mL BAN2401, 25 mmol/L histidine, 200 mmol/L arginine, and 0.05% polysorbate 80. In some embodiments, BAN2401, is formulated as disclosed in PCT/IB2021/000155 (WO2021/186245), which is incorporated herein by reference. In some embodiments, the composition comprises 80 mg/mL to 240 mg/mL BAN2401, 140 mM to 260 mM arginine hydrochloride, 0.01% w/v to 0.1% w/v polysorbate 80, and 15 mM to 35 mM histidine buffer. In some embodiments, the composition comprises a liquid dosage form comprising 200 mg/mL BAN2401, 25 mmol/L histidine, 200 mmol/L arginine, and 0.05% polysorbate 80. In some embodiments, provided herein is a method of treatment comprising administering a therapeutically effective dose of the anti-Aβ protofibril antibody until a desired improvement in one or more biomarkers is achieved, e.g. until an increase in the ratio of Aβ1-42 to Aβ1-40 in a fluid sample, e.g., a blood sample is observed and/or a decrease in the level of p-tau181 in a fluid sample, e.g., a blood sample is observed. In some embodiments, treatment is continued until a tau PET level has improved relative to an untreated control subject and/or treatment is continued until the ratio of Aβ1-42 to Aβ1-40 in a fluid sample, e.g., a blood sample is at or above 0.092. In some embodiments, treatment is continued until an amyloid PET or tau PET level has improved relative to an untreated control subject. In some embodiments, treatment is continued until a tau PET level has improved relative to an untreated control subject and/or the florbetapir amyloid PET SUVr negativity is below 1.17. In some embodiments, the one or more biomarkers comprises a serum or plasma GFAP measurement. In some embodiments, treatment is continued until a subject is amyloid negative. In some embodiments, a subject will switch to a maintenance dose after a desired improvement in one or more biomarkers is achieved. In some embodiments, a maintenance dosing regimen may further comprise one or more additional treatments in addition to an anti-Aβ protofibril antibody, e.g., it may comprise administering E2814. In some embodiments, provided herein is a method of treatment comprising administering a therapeutically effective dose of the anti-Aβ protofibril antibody until a desired improvement in the cognitive outcomes in a subject, e.g., one having Alzheimer’s disease, Pre-AD, or early Alzheimer’s disease, or other treatment outcome measures is achieved. In some embodiments, the method of Attorney Docket No.08061.0062-00304 treatment comprising administering a therapeutically effective dose of the anti-Aβ protofibril antibody for at least 18 months or e.g., until a desired improvement in the cognitive outcomes in a subject is achieved. Cognitive and functional decline can be measured by techniques known in the art, including scoring methods such as CDR-SB, ADCOMS Composite Clinical Score, the Mini-Mental State Examination, ADAS-Cog, ADAS MCI-ADL, modified iADRS, Wechsler Memory Scale-IV Logical Memory (subscale) I (WMS-IV LMI), and Wechsler Memory Scale-IV Logical Memory (subscale) II (WMS-IV LMII). In some embodiments, a method of treatment comprising administering a therapeutically effective dose of the anti-Aβ protofibril antibody continues until the method results in less cognitive decline as measured by ADCOMS compared to an untreated subject. In some embodiments, the efficacy of a method of treatment may be evaluated using a CDR global score, wherein a CDR global score may be used to determine if a patient has progressed or maintained a stage of AD during treatment, e.g., a higher score on a subsequent evaluation indicating progression of AD, e.g., an unchanged score indicating no progression of AD. In some embodiments, the method of treatment continues until the method results in at least 24% less (e.g., at least 29% less) cognitive decline as measured by ADCOMS compared to an untreated subject. In some embodiments, the method of treatment continues until the method results in less cognitive decline as measured by CDR- SB compared to an untreated subject. In some embodiments, the method of treatment continues until the method results in at least 26% less (e.g., at least 27% less) cognitive decline as measured by CDR- SB compared to an untreated subject. In some embodiments, the method of treatment continues until the method results in less cognitive decline as measured by ADAS-Cog14 compared to an untreated subject. In some embodiments, the method of treatment continues until the method results in at least 26% less (e.g., at least 47% less) cognitive decline as measured by ADAS-Cog14 compared to an untreated subject. In some embodiments, the method results in less cognitive decline as measured by ADCS MCI-ADL compared to an untreated subject. In some embodiments, the method results in at least 37% less cognitive decline as measured by ADCS MCI-ADL compared to an untreated subject. In some embodiments, the result is measured at least 6 months after administering a therapeutically effective amount of at least one anti-Aβ protofibril antibody. In some embodiments, the result is measured at least 12 months after administering a therapeutically effective amount of at least one anti- Aβ protofibril antibody. In some embodiments, the result is measured at least 13 months after administering a therapeutically effective amount of at least one anti-Aβ protofibril antibody. In some embodiments, the result is measured at least 18 months after administering a therapeutically effective amount of at least one anti-Aβ protofibril antibody. Methods of treatment, including dosing, by an intravenous administration of an anti-Aβ protofibril antibody are disclosed in PCT/US2022/073576 and PCT/US2022/079571 and are incorporated herein by reference. In some embodiments, a treatment comprises administering intravenously an anti-Aβ protofibril antibody at 10 mg/kg (e.g., administering BAN2401 at 10 Attorney Docket No.08061.0062-00304 mg/kg), biweekly, e.g., for at least 18 months or e.g., until a patient is amyloid-negative. In some embodiments, a treatment comprises administering intravenously an anti-Aβ protofibril antibody at 10 mg/kg (e.g., administering BAN2401 at 10 mg/kg), biweekly, e.g., for at least 18 months or e.g., until a patient is amyloid-negative, before switching to a maintenance dose. In some embodiments, the maintenance dose may be the same as the treatment dose, or it may involve a reduced dosage and/or frequency of administration. Methods of treatment, including dosing, by a subcutaneously administered anti-Aβ protofibril antibody are disclosed in PCT/US2022/073576; PCT/US2022/079571; and PCT/US2022/041926 and are incorporated herein by reference. In some embodiments, a treatment comprises subcutaneously administering an anti-Aβ protofibril antibody (e.g., administering BAN2401 at 720 mg), weekly, e.g., for at least 18 months or e.g., until a patient is amyloid negative. In some embodiments, a treatment comprises subcutaneously administering BAN2401 weekly, e.g., weekly subcutaneous injection of 720 mg in two concurrent, e.g., sequential, injections of 360 mg (2 x 1.8 mL of 400 mg/2 mL) of the subcutaneous formulation, e.g., until a patient is amyloid-negative or e.g., for at least 18 months. In some embodiments, a treatment comprises subcutaneously administering BAN2401 weekly, e.g., weekly subcutaneous injection of 720 mg in two concurrent, e.g., sequential, injections of 360 mg (2 x 1.8 mL of 400 mg/2 mL) of the subcutaneous formulation, e.g., until a patient is amyloid-negative or e.g., for at least 18 months. In some embodiments, a treatment comprises subcutaneously administering BAN2401 weekly, e.g., at a dose of 720 mg, e.g., for at least 18 months or e.g., until a patient is amyloid-negative, before switching to a weekly, subcutaneous maintenance dose, e.g., a dose of 360 mg. In some embodiments, a treatment comprises subcutaneously administering BAN2401 weekly, e.g., at a dose of 720 mg, e.g., for at least 18 months or e.g., until a patient is amyloid-negative, before switching to a biweekly subcutaneous maintenance dose, e.g., a dose of 720 mg. In some embodiments, the method of treatment comprises subcutaneously administering BAN2401 weekly, e.g., weekly subcutaneous injection of 720 mg in two concurrent, e.g., sequential, injections of 360 mg (2 x 1.8 mL of 400 mg/2 mL) of the subcutaneous formulation, e.g., for at least 18 months. In some embodiments, the method of treatment comprises subcutaneously administering BAN2401 weekly, e.g., weekly subcutaneous injection of 720 mg in two concurrent, e.g., sequential, injections of 360 mg (2 x 1.8 mL of 400 mg/2 mL) of the subcutaneous formulation, e.g., for at least 18 months, before switching to a maintenance dose. In some embodiments, the maintenance dose may be the same as the treatment dose, or it may involve a reduced dosage and/or frequency of administration. In some embodiments, the method of treatment comprises using a biomarker level, to determine switching to a maintenance intravenous or subcutaneous dose at a set time point (e.g., after 18 months). In some embodiments, a maintenance dose is administered subcutaneously (e.g., as one or more subcutaneous injections). In some embodiments, a treatment comprises administering intravenously an anti-Aβ protofibril antibody at 10 Attorney Docket No.08061.0062-00304 mg/kg (e.g., administering BAN2401 at 10 mg/kg), biweekly, before switching to a subcutaneous maintenance dose, e.g., a weekly subcutaneous maintenance dose, e.g., at 720 mg. In some embodiments, a treatment comprises administering intravenously an anti-Aβ protofibril antibody at 10 mg/kg biweekly before switching to a biweekly, 720 mg, subcutaneous maintenance dose. In some embodiments, the method of treatment comprises using a biomarker level to determine switching from a subcutaneous treatment to a maintenance dose. In some embodiments, a treatment comprises subcutaneously administering an anti-Aβ protofibril antibody, e.g., BAN2401, before switching to an intravenous maintenance dose. In some embodiments, a treatment comprises subcutaneously administering BAN2401 weekly, e.g., a subcutaneous injection of 720 mg comprising two concurrent, e.g., sequential, injections of 360 mg (2 x 1.8 mL of 400 mg/2 mL) before switching to a maintenance dose. In some embodiments, a treatment comprises subcutaneously administering BAN2401 weekly, e.g., at a dose of 720 mg before switching to a maintenance dose. In some embodiments, a treatment comprises subcutaneously administering BAN2401 weekly before switching to an intravenous maintenance dose of 10 mg/kg biweekly. In some embodiments, a subject’s maintenance dose is administered at the same amount and/or frequency as the dose during the treatment period. In some embodiments, a subject’s maintenance dose is 50% of the dose during the treatment period. In some embodiments, a patient starts on an intravenous maintenance dose, e.g., a dosing of 10 mg/kg BAN2401 as disclosed above before switching to a subcutaneous maintenance dose, e.g., a subcutaneous injection of 720 mg comprising two concurrent, e.g., sequential, injections of 360 mg (2 x 1.8 mL of 400 mg/2 mL) of the subcutaneous formulation. In some embodiments, a patient starts on a subcutaneous maintenance dose, e.g., a subcutaneous injection of 720 mg comprising two concurrent, e.g., sequential, injections of 360 mg (2 x 1.8 mL of 400 mg/2 mL) of the subcutaneous formulation before switching to an intravenous maintenance dose, e.g., a dosing of 10 mg/kg BAN2401 as disclosed above. In some embodiments, a patient is moved back from a maintenance dose to the initial treatment dose if the patient is determined to no longer be amyloid negative, e.g., as assessed by blood, serum, or CSF biomarker and/or as determined by amyloid PET SUVr. In some embodiments, a subject’s maintenance dose is administered at the same amount and/or frequency as the dose during the treatment period. In some embodiments, a subject’s maintenance dose is 50% of the dose during the treatment period. In some embodiments, the maintenance dose comprises two or more dosings, in which a first dosing is selected from the maintenance dose as exemplified above and a second and/or subsequent dosing comprising a lower amount and/or frequency of dosing than the first or previous dosing, respectively. In some embodiments, the switching to the second or subsequent dosing is determined based on one or more Attorney Docket No.08061.0062-00304 biomarkers as exemplified above, where the levels of the biomarkers are different from (e.g., improved over) the levels used in switching from initial dose to the first dosing in the maintenance dose. In some embodiments, a patient’s treatment is discontinued if a patient no longer has early AD, e.g., as assessed by cognitive evaluation, PET SUVr, and/or blood, CSF, or plasma biomarkers. In some embodiments, a patient’s amyloid level may be monitored for regression after treatment discontinuation by measuring a tau PET level and one or more biomarkers such as volumetric MRI (vMRI), comprising whole brain volume, cortical thickness, and/or total hippocampal volume. In some embodiments, a patient’s amyloid level may be monitored for regression after treatment discontinuation by measuring a tau PET level and one or more biomarkers such as a PET level, comprising an amyloid PET level and/or a fluorodeoxyglucose (FDG) PET level. In some embodiments, a patient’s amyloid level may be monitored for regression after treatment discontinuation by measuring a tau PET level and one or more biomarkers such as a cerebrospinal fluid level of a biomarker comprising the CSF level of Aβ1-42, Aβ1-40 (including a ratio of Aβ1-42 to Aβ1-40), total tau, p-tau (e.g, p-tau181, p-tau217, and/or p-tau231), the ratio of p-tau181/np- tau181, the ratio of p-tau217/np-tau217), neurogranin, and/or neurofilament light (NfL) peptide. In some embodiments, a patient’s amyloid level may be monitored for regression after treatment discontinuation by measuring a tau PET level and one or more biomarkers such as a serum or plasma level of a biomarker comprising Aβ1-42, Aβ1-40 (including a ratio of Aβ1-42 to Aβ1-40), total tau, phosphorylated tau (P-tau) (including tau phosphorylated at 181 (P-tau181), 217 (P-tau217), and/or 231 (P-tau231), the ratio of p-tau181/np-tau181, and/or the ratio of p-tau217/np-tau217, glial fibrillary acidic protein (GFAP), and/or neurofilament light (NfL). In some embodiments, a patient’s biomarkers may be monitored at least once after the discontinuation of treatment. In some embodiments, a patient’s biomarkers are monitored at least 1 week, 2 weeks, 3 weeks, 1 month, 2 months, 3 months, 6 months, 12 month, 18 months, or 24 months after treatment discontinuation. In some embodiments, treatment is reinitiated if a patient’s biomarker level becomes less favorable, e.g., a tau PET level increases at the same rate as an untreated control. In some embodiments, the subject has been diagnosed with early AD. In some embodiments, the subject has been diagnosed as having mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood and/or has been diagnosed as having mild Alzheimer’s disease dementia. Methods of treatment using an anti-Aβ protofibril antibody, including a therapeutically effective dosage, are disclosed in PCT/US2022/073576; PCT/US2022/079571; and PCT/US2022/041926, which is herein incorporated by reference. In some embodiments, the method of treatment comprises using a biomarker level, e.g., a tau PET level or a rate of change in a tau PET Attorney Docket No.08061.0062-00304 level, to allow for monitoring and treatment decisions, e.g., altering a dosage of BAN2401 and/or discontinuing treatment. 1. Definitions The following are definitions of terms used in the present application. As used herein, the singular terms “a,” “an,” and “the” include the plural reference unless the context clearly indicates otherwise. The phrase “and/or,” as used herein, means “either or both” of the elements so conjoined, i.e., elements that are conjunctively present in some cases and disjunctively present in other cases. Thus, as a non-limiting example, “A and/or B”, when used in conjunction with open-ended language such as “comprising” can refer, in some embodiments, to A only (optionally including elements other than B); in other embodiments, to B only (optionally including elements other than A); in yet other embodiments, to both A and B (optionally including other elements); etc. As used herein, “at least one” means one or more of the elements in the list of elements, but not necessarily including at least one of each and every element specifically listed within the list of elements and not excluding any combinations of elements in the list of elements. This definition also allows that elements may optionally be present other than the elements specifically identified within the list of elements to which the phrase “at least one” refers, whether related or unrelated to those elements specifically identified. Thus, as a non-limiting example, “at least one of A and B” (or, equivalently, “at least one of A or B,” or, equivalently “at least one of A and/or B”) can refer, in one embodiment, to at least one, optionally including more than one, A, with no B present (and optionally including elements other than B); in another embodiment, to at least one, optionally including more than one, B, with no A present (and optionally including elements other than A); in yet another embodiment, to at least one, optionally including more than one, A, and at least one, optionally including more than one, B (and optionally including other elements); etc. As used herein, “about” when used in connection with doses, amounts, or ratios, include the value of a specified dose, amount, or ratio or a range of the dose, amount, or ratio that is recognized by one of ordinary skill in the art to provide a therapeutic effect equivalent to that obtained from the specified dose, amount, or ratio. The term “about” may refer to an acceptable error for a particular value as determined by one of skill in the art, which depends in part on how the values is measured or determined. In some embodiments, the term “about” means within 5% of a given value or range. When a number is recited, either alone or as part of a numerical range, it should be understood that the numerical value can vary above and below the stated value by up to a variance of +/- 10% of the stated value. Attorney Docket No.08061.0062-00304 When a range of values is listed herein, it is intended to encompass each value and sub- range within that range. For example, “2.5 mg/kg to 10 mg/kg” is intended to encompass, for example, 2.5 mg/kg, 3 mg/kg, 3.5 mg/kg, 4 mg/kg, 4.5 mg/kg, 5 mg/kg, 5.5 mg/kg, 6 mg/kg, 6.5 mg/kg, 7 mg/kg, 7.5 mg/kg, 8 mg/kg, 8.5 mg/kg, 9 mg/kg, 9.5 mg/kg, 10 mg/kg, 2.5 mg/kg to 3 mg/kg, 2.5 mg/kg to 4.5 mg/kg, 3 mg/kg to 4.5 mg/kg, 4.5 mg/kg to 8 mg/kg, 2.5 mg/kg to 9 mg/kg, and so forth. As used herein, “adjusted mean change from baseline” refers to the use of a statistical analysis to calculate the change in a biomarker value over time. In some embodiments, a linear mixed-effects model (MMRM) is used to account for at least one additional covariate to determine the adjusted mean change from baseline. As used herein, “baseline” refers to an initial measurement (e.g., a measure of cognitive function, a brain structure, amyloid burden, and/or a fluid biomarker) taken at a first or an early time point and used for comparison over time to evaluate changes in the measurement. A change in a measurement over time as compared to a baseline may be used to assess the progression of a disease and/or the effect of a treatment for the disease. Amyloid β 1-42 (Aβ42) refers to an amyloid beta monomer from amino acid 1 to 42 of the full-length protein (Table 5, SEQ ID NO:13). Amyloid β 1-40 (Aβ1-40) refers to an amyloid beta monomer from amino acid 1 to 40 of the full-length protein (Table 5, SEQ ID NO:14). P-tau181 (also p-Tau181 or p-tau181) is human tau protein phosphorylated at threonine in position 181. NP-tau181 (also np-Tau181 or np-tau181) refers to human tau which is not phosphorylated at threonine in position 181. P-Tau181/NP-Tau181 (p-Tau181/np-Tau181, p- tau181/np-tau181, P-Tau181R, p-Tau181R, or p-tau181R) may refer to the ratio of tau phosphorylated at threonine in position 181 to non-phosphorylated tau at threonine in position 181. P-tau217 (also p-Tau217 or p-tau217) is human tau protein phosphorylated at threonine in position 217. NP-Tau217 (also np-Tau 217 or np-tau217) refers to human tau which is not phosphorylated at threonine in position 217. P-Tau217/NP-Tau217 (also p-Tau217/np-Tau217, p- tau217/np-tau217, P-Tau217R, p-Tau217R, or p-tau217R) may refer to the ratio of tau phosphorylated at threonine in position 217 to non-phosphorylated tau at threonine in position 217. P-tau231 (also p-Tau231 or p-tau231) is human tau protein phosphorylated at threonine in position 231. NP-Tau231(also np-Tau 231or np-tau231) refers to human tau which is not phosphorylated at threonine in position 231. P-Tau231/NP-Tau231 (also p-Tau231/np-Tau231, p- tau231/np-tau231, P-Tau231R, p-Tau231R, or p-tau231R) may refer to the ratio of tau phosphorylated at threonine in position 231 to non-phosphorylated tau at threonine in position 231. Attorney Docket No.08061.0062-00304 Total tau or t-tau as used herein is a measure of total tau in a sample, e.g. a CSF sample, a plasma sample, a serum sample. Patients (also called “subjects”) with “preclinical AD” or “pre-AD” as described herein, are cognitively normal individuals with intermediate or elevated levels of amyloid in the brain and can be identified by asymptomatic stages with or without memory complaints and emerging episodic memory and executive function deficits. Such patients may be identified by one or more biomarker. Cognitively normal can include individuals who are CDR 0, or individuals within the normal ranges of cognitive test scores (MMSE, International Shopping List Task, Logical Memory, etc.). Preclinical AD occurs prior to significant irreversible neurodegeneration and cognitive impairment and is typically characterized by the appearance of in vivo molecular biomarkers of AD and the absence of clinical symptoms. Preclinical AD biomarkers that may suggest the future development of Alzheimer’s disease include, but are not limited to, one or more of intermediate or elevated levels of amyloid in the brain by amyloid, fluorodeoxyglucose (FDG), or tau positron emission tomography (PET) (e.g., a centiloid measure of about 20-40, e.g., a measure of about 20-32), cerebrospinal fluid level of Aβ1-42 and/or Aβ1-42/1-40 ratio, cerebrospinal fluid level of total tau, cerebrospinal fluid level of p-tau (including tau phosphorylated at 181 (P-tau181), 217 (P-tau217), and/or 231 (P-tau231), the ratio of P-tau181/NP-tau181, and/or the ratio of P-tau217/NP-tau217), cerebrospinal fluid level of neurogranin, cerebrospinal fluid level of neurofilament light peptide (NfL), and blood biomarkers as measured in the serum or plasma (e.g. levels of Aβ1-42, the ratio of two forms of amyloid-β peptide (Aβ1-42/1-40 ratio, e.g., a ratio of between about 0.092-0.094 or below about 0.092), plasma levels of plasma total tau (T-tau), levels of phosphorylated tau (P-tau) isoforms (including tau phosphorylated at 181 (P-tau181), 217 (P-tau217), and/or 231 (P-tau231)), the ratio of P-tau181/NP-tau181, and/or the ratio of P-tau217/NP-tau217), glial fibrillary acidic protein (GFAP), and neurofilament light (NfL)). For example, it has been found that subjects treated with elenbecestat (E2609), a β-site amyloid precursor protein cleaving enzyme (BACE) inhibitor, who had amyloid baseline positron emission tomography (PET) standard uptake value ratios (SUVr values) of 1.4 to 1.9, exhibited the greatest slowing of cognitive decline while on treatment. See Lynch, S. Y. et al. “Elenbecestat, a BACE inhibitor: results from a Phase 2 study in subjects with mild cognitive impairment and mild-to- moderate dementia due to Alzheimer’s disease.” Poster P4-389, Alzheimer’s Association International Conference, July 22-26, 2018, Chicago, IL, USA. Similarly, it has been found that subjects having a baseline florbetapir amyloid PET SUVr levels below 1.2 do not exhibit enough cognitive decline to be detectable, whereas subjects having SUVr levels above 1.6 appear to correlate with a plateau effect in which amyloid level has reached a saturation level and treatment does not result in a change of cognitive measures. See Dhadda, S. et al., “Baseline florbetapir amyloid PET standard update value ratio (SUVr) can predict clinical progression in prodromal Alzheimer’s disease Attorney Docket No.08061.0062-00304 (pAD).” Poster P4-291, Alzheimer’s Association International Conference, July 22-26, 2018, Chicago, IL, USA. “Early AD” or “early Alzheimer’s disease,” as used herein, is a continuum of AD severity from mild cognitive impairment due to AD – intermediate likelihood to mild Alzheimer’s disease dementia. Subjects with early AD include subjects with mild Alzheimer’s disease dementia as defined herein and subjects with mild cognitive impairment (MCI) due to AD – intermediate likelihood as defined herein. In some embodiments, subjects with early AD have MMSE scores of 22 to 30 and Clinical Dementia Rating (CDR) global range 0.5 to 1.0. Other methods for detecting early AD disease may employ the tests and assays specified below, including the National Institute of Aging- Alzheimer’s Association (NIA-AA) core clinical criteria for probable Alzheimer’s disease dementia in McKhann, G.M. et al., “The diagnosis of dementia due to Alzheimer’s disease: Recommendations from the National Institute on Aging – Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease.” Alzheimer Dement.2011; 7:263-9. Other methods include CDR-SB, ADCOMS Composite Clinical Score, the Mini-Mental State Examination, ADAS-Cog, ADAS MCI- ADL, modified iADRS, Wechsler Memory Scale-IV Logical Memory (subscale) I (WMS-IV LMI), and Wechsler Memory Scale-IV Logical Memory (subscale) II (WMS-IV LMII). In some embodiments, a subject with early AD has evidence of elevated amyloid in the brain or a positive amyloid load. In some embodiments, elevated amyloid in the brain or a positive amyloid load is indicated and/or confirmed by PET assessment. In some embodiments, elevated amyloid in the brain or a positive amyloid load is indicated and/or confirmed by a CSF assessment of markers such as Aβ1-42 (e.g., a soluble CSF biomarker analysis). In some embodiments, elevated amyloid in the brain or a positive amyloid load is indicated and/or confirmed by measuring the level of p-tau181. In some embodiments, elevated amyloid in the brain or a positive amyloid load is indicated and/or confirmed by an MRI. In some embodiments, elevated amyloid in the brain or a positive amyloid load is indicated by retinal amyloid accumulation. In some embodiments, more than one assessment method is used. “Amyloid” refers to fibers that are unbranched, usually extracellular, and found in vivo; in addition, the fibers bind the dye Congo Red and then show green birefringence when viewed between crossed polarizers. Amyloid-forming proteins have been identified and associated with serious diseases, including amyloid-β peptide (Aβ) with Alzheimer’s disease (AD), islet amyloid polypeptide (IAPP) with diabetes type 2, and prion protein (PrP) with the spongiform encephalopathies. As used herein, “amyloid,” “brain amyloid,” and “amyloid-β peptide (Aβ)” are used interchangeably. In some embodiments, the subject has “elevated amyloid” or “intermediate amyloid.” As one of ordinary skill in the art will recognize, amyloid levels from amyloid PET can be reported using the Centiloid method in “centiloid” units (CL). (Klunk WE et al. The Centiloid Project: standardizing Attorney Docket No.08061.0062-00304 quantitative amyloid plaque estimation by PET. Alzheimer’s Dement.2015; 11:1–15 e1–4). The Centiloid method measures a tracer on a scale of 0 CL to 100 CL, where 0 is deemed the anchor-point and represents the mean in young healthy controls and 100 CL represents the mean amyloid burden present in subjects with mild to moderate severity dementia due to AD. (Id.) As is known to one of ordinary skill in the art, centiloid thresholds may vary, for example may be refined, based on new or additional scientific information. (See, e.g., http://www.gaain.org/centiloid-project.) An elevated level of amyloid can be set relative to a baseline threshold in a healthy control determined according to methods known to a person of ordinary skill in the art (POSA). For example, a centiloid value of 32.5 can be used as a threshold value for “elevated amyloid,” and an “intermediate amyloid” level refers to an Aβ amyloid PET in the range of 20-32.5 CL (e.g., 30 CL). In another example, a centiloid value of 40 can be used as a threshold value for “elevated amyloid,” and an “intermediate amyloid” level refers to an Aβ amyloid PET in the range of 20-40 CL. Subjects with “mild Alzheimer’s disease dementia,” or “mild AD dementia” as used herein, are subjects meeting the National Institute of Aging-Alzheimer’s Association (NIA-AA) core clinical criteria for probable Alzheimer’s disease dementia in McKhann, G.M. et al., “The diagnosis of dementia due to Alzheimer’s disease: Recommendations from the National Institute on Aging – Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease.” Alzheimer Dement.2011; 7:263-9. Also included herein are subjects who have a CDR score of 0.5 to 1.0 and a Memory Box score of 0.5 or greater at screening and baseline and subjects that exhibit change in the score on the Wechsler Memory Scale-IV Logical Memory (subscale) II (WMS-IV LMII). Subjects with “MCI due to AD – intermediate likelihood,” as used herein are those identified as such in accordance with the NIA-AA core clinical criteria for mild cognitive impairment due to Alzheimer’s disease – intermediate likelihood (see McKhann supra). For example, a subject may be symptomatic but not demented, with evidence of brain amyloid pathology making them less heterogeneous and more similar to mild Alzheimer’s disease dementia subjects in cognitive and functional decline as measured by the ADCOMS Composite Clinical Score defined herein. Also included are subjects who have a CDR score of 0.5 and a Memory Box score of 0.5 or greater at screening and baseline. Furthermore, subjects who report a history of subjective memory decline with gradual onset and slow progression over the last 1 year before screening, which is corroborated by an informant, are also included herein. Memory decline and/or episodic memory impairment can be assessed in a subject by change in the score on the Wechsler Memory Scale-Revised Logical Memory subscale II (WMS-R LM II). As used herein, a “control subject”, “untreated AD subject”, or an “untreated control subject” is a subject that is not being treated or has been treated for Alzheimer’s disease. In some embodiments, a control subject has Alzheimer’s disease. In some embodiments, the control subject Attorney Docket No.08061.0062-00304 has early Alzheimer’s disease, or pre-Alzheimer’s disease. In some embodiments, the control subject has Alzheimer’s disease and is not treated with an anti-Aβ protofibril antibody. The terms “patient” and “subject” are used interchangeably. As used herein, “MMSE” refers to the Mini-Mental State Examination, a cognitive instrument commonly used for screening purposes, but also often measured longitudinally in AD clinical trials having a 30 point scale with higher scores indicating less impairment and lower scores indicating more impairment, ranging from 0 (most impaired) to 30 (no impairment). In some embodiments, seven items measuring orientation to time and place, registration, recall, attention, language, and drawing may be assessed as part of the MMSE score. (Folstein, M.F. et al., “Mini- mental state. A practical method for grading the cognitive state of patients for the clinician.” J. Psychiatr. Res.1975;12:189-98.) As used herein, “ADAS-Cog” refers to Alzheimer’s Disease Assessment Scale-Cognitive. The ADAS-Cog is a widely used cognitive scale in Alzheimer's disease trials having a structured scale that evaluates memory (word recall, delayed word recall, and word recognition), reasoning (following commands), language (naming, comprehension), orientation, ideational praxis (placing letter in envelope) and constructional praxis (copying geometric designs). (Rosen, W.G. et al., “A new rating scale for Alzheimer’s disease.” Am. J. Psychiatry 1984; 141:1356-64.) Ratings of spoken language, language comprehension, word finding difficulty, ability to remember test instructions, maze, and number cancellation may also be obtained. In some embodiments, ADAS-Cog refers to the use of the Alzheimer Disease Assessment Scale-Cognitive Subscale₁₄ (ADAS-Cog14). In some embodiments, a modified version may be used herein and is scored from 0 to 90 points with a score of 0 indicating no impairment, and a score of 90 indicating maximum impairment. In some embodiments, the ADAS–Cog14 tasks include memory (word recall, delayed word recall, and word recognition), reasoning (following commands), language (naming, comprehension), orientation, ideational praxis (placing letter in envelope), constructional praxis (copying geometric designs), spoken language, language comprehension, word finding difficulty, ability to remember test instructions, maze, and number cancellation (Rosen et al, 1984). As used herein, “CDR-SB” refers to clinical dementia rating - sum of boxes. The CDR is a clinical scale that describes 5 degrees of impairment in performance on each of 6 categories of function including memory, orientation, judgment and problem solving, community affairs, home and hobbies, and personal care. (Berg, L. et al., “Mild senile dementia of the Alzheimer type: 2. Longitudinal assessment.” Ann. Neurol.1988; 23:477-84.) A sum of boxes score provides a measure of change where each category has a maximum possible score of 3 points and the total score is a sum of the category scores giving a total possible score of 0 to 18 with higher scores indicating more impairment. Attorney Docket No.08061.0062-00304 As used herein, “CDR global”, “global CDR” score and “global rating of dementia CDR” score is used interchangeably. As used herein, CDR global score is a rating of the degree of impairment obtained on each of the 6 categories of function from the 6 categories of the CDR scaleand is synthesized into 1 global rating of dementia CDR score, (ranging from 0 to 3) where 0 indicates no cognitive impairment, 0.5 indicates mild cognitive impairment, and 1-3 indicates mild, moderate, severe dementia respectively. The global CDR score may be used as a clinical measure of severity of dementia. In some embodiments, a global CDR score may be used to determine if a patient has progressed or maintained a stage of AD, e.g., a higher score on a subsequent evaluation indicating progression of AD, e.g., an unchanged score indicating no progression of AD. As used herein, “ADCOMS” refers to Alzheimer’s Disease Composite Score, a composite clinical score based on an analysis of four ADAS-Cog items (delayed word recall, orientation, word recognition, and word finding difficulty), two Mini Mental State Examination (MMSE) items (orientation to time, and drawing), and all six CDR-SB items (personal care, community affairs, home and hobbies, memory, orientation, and judgment and problem solving), as discussed in the Examples and in Wang, J. et al., “ADCOMS: a composite clinical outcome for prodromal Alzheimer’s disease trials.” J. Neurol. Neurosurg. Psychiatry.2016; 87:993-999. ADCOMS was developed to be particularly sensitive to disease progression during early stages of AD (i.e., preclinical AD or early AD). In some embodiments, ADCOMS can be calculated using the following formula: ^^{ଶ ^ ^} ^^^ ^^^ ൌ ^ ^^_^ ^^_^^ ^^^ ^^ ^^_^ ^^_^^ ^^^ ^^ ^^_^ ^^_^^ ^^^ where ^^_^^ ^^^, ^^_^^ ^^^ and ^^_^^ ^^^

from ADAS-cog, reversed MMSE scores, and CDR-SB, respectively (Wang, J. et al., “ADCOMS: a composite clinical outcome for prodromal Alzheimer’s disease trials). ADCOMS is particularly sensitive to disease progression during early stages of AD, i.e., prodromal and mild AD. As used herein, “ADCS MCI-ADL” refers to the Alzheimer's Disease Cooperative Study- Activities of Daily Living Scale for Mild Cognitive Impairment (ADCS MCI-ADL). The ADCS MCI-ADL is a clinical scale that assesses the competence level of a patient at six basic activities of daily living. Additional examples are discussed in Kreutzer J.S., DeLuca J., Caplan B. (eds) Encyclopedia of Clinical Neuropsychology. Springer, New York, NY. As used herein, “modified iADRS” or “iADRS” refers to a composite tool that combines scores from the ADAS Cog14 (all items) and the ADCS MCI-ADL (all items). The modified iADRS score can be used to evaluate disease progression: Attorney Docket No.08061.0062-00304 Modified iADRS score = [-1(ADAS-cog14) +90] + ADCS MCI-ADL. As used herein, “ApoE4-positive” subjects and “ApoE4 carriers” refer to subjects who harbor the ε4 variant of the apolipoprotein (APOE) gene. As used herein, APOE4 status refers to a subject’s status as a gene carrier. The ε4 variant is one of several major alleles of the apolipoprotein gene. The gene is generally responsible for metabolism of fats. It has been found that carriers of the apolipoprotein ε4 show significantly greater rates of amyloid retention when compared to non- carriers. (Drzezga, A. et al, “Effect of APOE genotype on amyloid plaque load and gray matter volume in Alzheimer disease.” Neurology.2009; 72:1487-94.) In some embodiments, a subject treated herein is a heterozygous carrier of the apolipoprotein E ε4 gene allele. In some embodiments, the subject is a homozygous carrier of the apolipoprotein E ε4 gene allele. The terms “ApoE4- negative” and “ApoE4 non-carriers” are used interchangeably. As used herein, whether an early AD subject is “amyloid positive” or “amyloid negative” may be determined based on whether the subject has a positive amyloid load. In some embodiments, a subject is determined to be amyloid-positive or amyloid-negative as indicated by longitudinal positron emission tomography (PET) assessment of an imaging agent uptake into the brain, e.g., an amyloid imaging agent or a tau imaging agent. In some embodiments, a subject is determined to be amyloid- positive or amyloid-negative by evaluation of a tau PET imaging assessment. In some embodiments, a subject is “amyloid negative” if the florbetapir amyloid PET SUVr negativity is below 1.17. In some embodiments, a subject is determined to be amyloid-positive or amyloid-negative by evaluation of the level of a biomarker in a sample (e.g., a Aβ42/40 ratio) from a subject, alone or in combination with another method such as PET measurement of brain amyloid. In some embodiments, a subject is “amyloid negative” if the Aβ42/40 ratio in a sample is at or about above 0.092-0.094 e.g., at about 0.092. In some embodiments, a subject is “amyloid negative” if the Aβ42/40 ratio in a sample is above 0.092. In some embodiments, a subject is determined to be amyloid-positive or amyloid- negative by a CSF assessment of the presence of amyloid pathology using assessments of markers such as p-tau181, alone or in combination with another method such as PET measurement of brain amyloid. In some embodiments, a qualitative visual read of PET scans may be used to determine amyloid positive and amyloid negative by categorizing subjects as having either “normal” or “abnormal” uptake on the basis of the PET image pattern. Readers will have been trained and certified to recognize brain PET images with abnormal or normal patterns of uptake, or the detection of amyloid is done through a semi-quantitative or quantitative approach. In some embodiments, a threshold will be set for quantitatively determining from a biomarker (e.g., serum or CSF) and/or PET scan whether an Aβ brain load indicates a subject is amyloid-positive or negative. In some embodiments, a subject is determined to be amyloid-positive or amyloid-negative by an MRI. In some Attorney Docket No.08061.0062-00304 embodiments, a subject is determined to be amyloid-positive or amyloid-negative by retinal amyloid accumulation. In some embodiments, a subject is determined to be amyloid-positive or amyloid- negative by behavioral/cognitive phenotypes. As would be understood by one of ordinary skill in the art, digital, computerized, and/or conventional (e.g., pen and paper) cognitive tests may be used to detect early cognitive changes that may signal mild cognitive impairment and/or a risk for developing dementia, and thus may be used to identify subject in need of treatment as disclosed herein. Such tests, for example, may screen for cognitive impairment, and potentially identify individuals with MCI. Tests may use artificial intelligence to analyze cognitive test results to determine whether a case of mild cognitive impairment will escalate into Alzheimer’s within a year. Diagnosing the condition early, before symptoms have begun to appear, may be used to assist physicians identify subjects in need of treatment as disclosed herein sooner, potentially delaying onset or lessening the severity of the neurodegenerative disease. As used herein, the term “treat” refers to any administration or application of a therapeutic agent for a disease or disorder in a subject, and includes inhibiting the disease, slowing progression of the disease, delaying progression, arresting its development, reversing progression of disease (e.g., reversing build up of Aβ fibrils), preventing the onset or development of the disease, relieving or ameliorating one or more symptoms or underlying condition(s) of the disease, curing the disease, improving one or more clinical metrics, or preventing reoccurrence of one or more symptoms of the disease. In some embodiments, treatment of AD in a subject comprises an administration, e.g., an intravenous infusion, of an anti-amyloid β (Aβ) protofibril antibody. In some embodiments, treatment of AD in a subject comprises a therapeutically effective dose by administration, e.g., an intravenous infusion, of an anti-amyloid β (Aβ) protofibril antibody. As used herein, the term “infusion” refers to an active administration of one or more agents with an infusion time of, for example, approximately 60 minutes. In some embodiments, an anti-amyloid β(Aβ) protofibril antibody, described herein is systemically administered to a human subject via infusion. In some embodiments, an anti-amyloid β(Aβ) protofibril antibody is alternatively administered to the human subject, e.g., by subcutaneous injection. In some embodiments, the subcutaneous injection is a weekly injection. In some embodiments, the subcutaneous injection is a biweekly injection. In some embodiments, an anti-amyloid β(Aβ) protofibril antibody is administered to the human subject by intravenous infusion. In some embodiments, the subject is administered a maintenance dose of a treatment. As used herein, the term “maintenance dose” refers to a dosage administered to a subject to maintain the desired therapeutic effect. In some embodiments, the maintenance dose is administered weekly, every two weeks, monthly, every two months, or every three months (quarterly) or every 24 weeks (every six months or semi-annually). In some embodiments, the maintenance dose comprises an anti-Aβ Attorney Docket No.08061.0062-00304 protofibril antibody. In some embodiments, the maintenance dose is administered as an intravenous infusion. In some embodiments, the intravenous infusion is a 10 mg/kg dose of BAN2401 administered biweekly. In some embodiments, the intravenous infusion is a 10 mg/kg dose of BAN2401 administered monthly. In some embodiments, the maintenance dose is administered subcutaneously, orally, or nasally. In some embodiments, the maintenance dose is administered subcutaneously. In some embodiments, the maintenance dose is administered as a subcutaneous injection. In some embodiments, the maintenance dose is administered as a weekly, subcutaneous injection. In some embodiments, the maintenance dose is administered as a biweekly, subcutaneous injection. In some embodiments, the maintenance dose is administered as a monthly, subcutaneous injection. In some embodiments, the maintenance dose is administered as a quarterly, subcutaneous injection. In some embodiments, the maintenance dose is administered weekly or less frequently, e.g., every two weeks (biweekly), every four weeks, monthly, every six weeks, every eight weeks (2 months), every three months (quarterly) or every six monthly (semi-annually). In some embodiments, the maintenance dose is administered as a biweekly, subcutaneous injection of 720 mg. In some embodiments, the maintenance dose is administered as a biweekly, subcutaneous injection of 720 mg comprising two concurrent, e.g., sequential, injections of 360 mg (2 x 1.8 mL of 400 mg/2 mL) of the subcutaneous formulation. In some embodiments, the maintenance dose is administered as a weekly, subcutaneous injection of 250 mg. In some embodiments, the maintenance dose is administered as a weekly, subcutaneous injection of 250 mg comprising injection of 1.25 mL of 400 mg/2 mL of a subcutaneous formulation. In some embodiments, the maintenance dose is administered as a weekly, subcutaneous injection of 360 mg comprising a single injection of 360 mg of the SC formulation. In some embodiments, the maintenance dose is administered subcutaneously from an autoinjector. In some embodiments, the maintenance dose is administered as a biweekly, subcutaneous injection of 720 mg or 500 mg. In some embodiments, the maintenance dose is administered as a biweekly, subcutaneous injection of 500 mg comprising two concurrent, e.g., sequential, injections of 250 mg (e.g., 2 x 1.25 mL of 400 mg/2 mL) of the subcutaneous formulation. In some embodiments, the maintenance dose is administered as a biweekly, subcutaneous injection of 500 mg comprising a single injection of 500 mg (e.g., 2.5 mL of 400 mg/2 mL) of the SC formulation. In some embodiments, the maintenance dose is administered subcutaneously from an autoinjector. In some embodiments, the maintenance dose is administered once or multiple times. In some embodiments, the maintenance dose is administered at a lower dose than during an earlier course of treatment and/or is administered less frequently than during the earlier course of treatment. Attorney Docket No.08061.0062-00304 In some embodiments, after switching to a maintenance dose, a subject’s biomarker levels may indicate increasing levels of amyloid in the brain. In some embodiments, after switching to a maintenance dose, a subject’s biomarker levels may begin to worsen, e.g. an increasing plasma Aβ42/40 ratio, indicating increasing levels of amyloid in the brain. In some embodiments, a subject on a maintenance dose may have a decrease in the Aβ42/40 ratio. In some embodiments, a subject is put on a maintenance dose chosen such that the subject may have a decrease in the Aβ42/40 ratio but the Aβ42/40 ratio may remain above the threshold for amyloid positivity, e.g. for at least one year (e.g., at least 1, 2, 3, 4, 5, 6, 7, 8, 9, or 10 years). In some embodiments, after switching to a maintenance dose, a subject’s biomarker levels may begin to increase or a rate of increase may increase. In some embodiments, such a subject may be moved back to a treatment regimen. In some embodiments, a subject may remain on a maintenance dose, e.g., if the increase remains below a tau PET level or rate of increase seen in a control subject who has AD but does not receive an anti-Aβ protofibril antibody. As used herein, the term “prevent” refers to obtaining beneficial or desired results including, but not limited to, prophylactic benefit. For prophylactic benefit, the composition may be administered to a subject at risk of developing Alzheimer’s disease, to a subject having one or more preclinical symptoms but not clinical symptoms of Alzheimer’s disease, or to a subject reporting one or more of the physiological symptoms of Alzheimer’s disease, even though a clinical diagnosis of having Alzheimer’s has not been made. As used herein “prevention” may further include therapeutic benefit, by which is meant eradication or amelioration of the underlying condition being treated or of one or more of the physiological symptoms associated therewith. As used herein, the term “ARIA” refers to amyloid-related imaging abnormality as evaluated using MRI. Without being bound by theory, ARIA may be a consequence of the presence of amyloid in cerebral blood vessel walls, resulting in cerebral amyloid angiopathy (CAA). Without being bound by theory, CAA is present pathologically in most patients with Alzheimer’s, but most patients show no imaging findings (microhemorrhage) or clinical manifestations (intracerebral hemorrhage or inflammatory CAA). Without being bound by theory, removal of amyloid by monoclonal antibodies, e.g., an anti-Aβ protofibril antibody, may increase the risk of ARIA. In some embodiments, ARIA includes amyloid related imaging abnormality edema/effusion (ARIA-E). In some embodiments, ARIA includes amyloid related imaging abnormality hemorrhage (ARIA-H). In some embodiments, the severity of ARIA may be categorized by radiographic imaging, e.g., MRI. In some embodiments, the severity of ARIA may be categorized as mild, moderate, or severe based on radiographic imaging, e.g., MRI. In some embodiments, a mild ARIA-E event comprises FLAIR hyperintensity confined to sulcus and/or cortex/subcortex white matter in one location <5 cm. In some embodiments, a moderate ARIA-E comprises FLAIR hyperintensity 5 to 10 cm in single greatest Attorney Docket No.08061.0062-00304 dimension, or more than 1 site of involvement, each measuring <10 cm. In some embodiments, a severe ARIA-E event comprises FLAIR hyperintensity >10 cm with associated gyral swelling and sulcal effacement, and one or more separate/ independent sites of involvement may be noted. In some embodiments, a mild ARIA-H microhemorrhage event comprises ≤ 4 new incident microhemorrhages. In some embodiments, a moderate ARIA-H microhemorrhage event comprises 5 to 9 new incident microhemorrhages. In some embodiments, a severe ARIA-H microhemorrhage event comprises 10 or more new incident microhemorrhages. In some embodiments, a mild ARIA-H superficial siderosis event comprises 1 focal area of superficial siderosis. In some embodiments, a moderate ARIA-H superficial siderosis event comprises 2 focal areas of superficial siderosis. In some embodiments, a severe ARIA-H superficial siderosis event comprises > 2 areas of superficial siderosis. In some embodiments, ARIA-H may include intracerebral hemorrhages > 1 cm. As used herein, the term “clinical decline” refers to a worsening of one or more clinical symptoms of AD. Methods for measuring clinical decline may employ the tests and assays specified herein. In some embodiments, clinical decline is determined by a worsening of ADCOMS. In some embodiments, clinical decline is determined by a worsening of MMSE. In some embodiments, clinical decline is determined by a worsening of ADAS-Cog. In some embodiments, clinical decline is determined by a worsening of FAQ. In some embodiments, clinical decline is determined by a worsening of CDR-SB. In some embodiments, clinical decline is determined by a worsening of Wechsler Memory Scale-IV Logical Memory (subscale) I and/or (subscale) II. In some embodiments, clinical decline is determined by a worsening of CDR score. In some embodiments, clinical decline refers to a worsening in one or more biomarkers of AD or brain measurement (e.g., by PET or MRI), e.g., of brain atrophy and/or amyloid accumulation. As used herein, the term “blood sample” or “blood” refers to a sample of blood, including serum and/or blood plasma from a human subject. In some embodiments, blood will be collected from subjects to evaluate potential biomarkers of AD that may include amyloid fragments and isoforms, tau, and other protein biomarkers (e.g., NFL) for association with AD diagnosis, amyloid or tau load, or disease modification. In some embodiments, subjects are required to fast if possible before collection at Week 96 and Week 216. In other embodiments and/or at other time points, subjects do not require fasting. Pre-AD biomarker levels that may suggest the development of Alzheimer’s disease include, but are not limited to, brain amyloid level, cerebrospinal fluid level of Aβ1-42, cerebrospinal fluid level of total tau, cerebrospinal fluid level of neurogranin, and cerebrospinal fluid level of neurofilament light chain (NfL). 2. Measurement of ARIA The disclosure and methods discussed herein turn in part on the discovery that the risk of an amyloid related imaging abnormality (ARIA) from treatment with anti-Aβ protofibril antibody Attorney Docket No.08061.0062-00304 such as BAN2401, may depend upon the concomitant use of other medications, such as anticoagulants or thrombolytics, or the presence of brain hemorrhages and status of the brain at baseline. In some embodiments, amyloid related imaging abnormalities (ARIA) can be measured by tools known in the art and may include those described herein. In some embodiments, ARIA is measured by MRI. In some embodiments, ARIA is categorized as ARIA with edema (ARIA-E) or hemosiderin deposition (ARIA-H). In some embodiments, ARIA-E maybe observed on MRI as brain edema or sulcal effusions. In some embodiments, ARIA-H may be observed on MRI as brain microhemorrhages or superficial siderosis. In some embodiments, a patient is monitored for ARIA prior to treatment, e.g., treatment with anti-Aβ protofibril antibody, e.g., treatment with BAN2401, by radiographic imaging (e.g., MRI). In some embodiments, a patient is monitored for ARIA at least once after treatment, e.g., treatment with anti-Aβ protofibril antibody, e.g., treatment with BAN2401, by radiographic imaging (e.g., MRI). In some embodiments, a patient is monitored for ARIA more than once after treatment, e.g., treatment with anti-Aβ protofibril antibody, e.g., treatment with BAN2401, by radiographic imaging (e.g., MRI). In some embodiments, a patient is monitored for ARIA may be monitored at least once after the discontinuation of treatment. In some embodiments, a patient is monitored for ARIA at least 1 week, 2 weeks, 3 weeks, 1 month, 2 months, 3 months, 6 months, 12 month, 18 months, or 24 months after treatment discontinuation. In some embodiments, subjects with ARIA experience headache, confusion, and/or seizure and these may be used to identify a subject with ARIA or to indicate further evaluation for ARIA. In some embodiments, ARIA is evaluated at specified intervals during treatment. In some embodiments, ARIA is evaluated when the subject experiences symptoms of ARIA. In some embodiments, maximum serum concentration (Cmax) of anti-Aβ protofibril antibody can be used as a predictor of the risk of ARIA-E. In some embodiments, the use of a subcutaneous formulation may provide a reduced risk of ARIA-E (e.g., due to a lower Cmax) compared to an IV administration. In some embodiments, ARIA may be classified by clinical symptom severity. For example, mild clinical symptom severity may be characterized by discomfort that is noticed, but there is no disruption of normal daily activity. Moderate clinical symptom severity may be characterized by discomfort sufficient to reduce or affect normal daily activity. Severe clinical symptom severity may be incapacitating, leading to an ability to work or to perform normal daily activity. In some embodiments, ARIA may be classified by radiographic severity, e.g., by extent of signal abnormality in MRI. In some embodiments, the radiographic severity depends on signal abnormalities on T2 weighted/fluid attenuation inversion recovery (FLAIR) sequences. In some embodiments, radiographic severity in ARIA-E may be classified as mild if FLAIR hyperintensity is Attorney Docket No.08061.0062-00304 confined to sulcus and/or cortex/subcortex white matter in one location <5 cm. In some embodiments, radiographic severity in ARIA-E may be classified as moderate if FLAIR hyperintensity is 5 to 10 cm in single greatest dimension, or more than 1 site of involvement, each measuring <10 cm. In some embodiments, radiographic severity in ARIA-E may be classified as severe if FLAIR hyperintensity is >10 cm with associated gyral swelling and sulcal effacement. One or more separate/ independent sites of involvement may be noted. In some embodiments, ARIA may be classified by radiographic severity, e.g., by the number and/or size of microhemorrhages, and/or by the number and/or size of focal areas of superficial siderosis. In some embodiment, radiographic severity in ARIA-H (microhemorrhage) may be classified as mild if there are ≤ 4 new incident microhemorrhages. In some embodiments, radiographic severity in ARIA-H (microhemorrhage) may be classified as moderate if there are 5 to 9 new incident microhemorrhages. In some embodiments, radiographic severity in ARIA-H (microhemorrhage) may be classified as severe if there are 10 or more new incident microhemorrhages. In some embodiments, radiographic severity in ARIA-H (superficial siderosis) may be classified as mild if there is 1 focal area of superficial siderosis. In some embodiments, radiographic severity in ARIA-H (superficial siderosis) may be classified as moderate if there are 2 focal areas of superficial siderosis. In some embodiments, radiographic severity in ARIA-H (superficial siderosis) may be classified as severe if > 2 areas of superficial siderosis. In some embodiments, treatment with an anti-Aβ protofibril antibody such as BAN2401 may be continued if the clinical symptom severity and the radiographic severity are mild. For example, for ARIA-E, if the clinical symptom severity is asymptomatic and the radiographic severity is mild, the treatment may be continued. In some embodiments, for ARIA-E, if the clinical symptom severity is mild and the radiographic severity is mild, the treatment may continue based on clinical judgment. In some embodiments, for ARIA-E, if the clinical symptom severity is moderate or severe, the treatment may be suspended. In some embodiments, for ARIA-E, if the radiographic severity is moderate or severe, the treatment may be suspended. In some embodiments, a treatment may be suspended until MRI demonstrates radiographic resolution and symptoms, if present, resolve. A follow-up MRI may be performed to assess for resolution 2-4 months after initial identification of ARIA. In some embodiments, after radiographic stabilization and resolution of symptoms, if any, the treatment may be resumed. In some embodiments, the treatment may be permanently discontinued. In some embodiments, for ARIA-H, if the clinical symptom severity is asymptomatic and the radiographic severity is mild, the treatment may be continued. In some embodiments, for ARIA- H, if the clinical symptom severity is symptomatic, the treatment may be suspended, whether the radiographic severity is mild, moderate, or severe. In some embodiments, a treatment may be Attorney Docket No.08061.0062-00304 suspended until MRI demonstrates radiographic resolution and symptoms, if present, resolve. A follow-up MRI may be performed to assess for resolution 2-4 months after initial identification of ARIA. In some embodiments, after radiographic stabilization and resolution of symptoms, if any, the treatment may be resumed. In some embodiments, the treatment may be permanently discontinued. 3. Measurement of Brain Hemorrhage The disclosure and methods discussed herein turn in part on the discovery that the risk of brain hemorrhage (e.g., microhemorrhage, intracerebral hemorrhage) from treatment with anti-Aβ protofibril antibody such as BAN2401, may depend upon the presence of brain hemorrhages and status of the brain at baseline. In some embodiments, a patient with a brain hemorrhage, e.g., an intracerebral hemorrhage, a microhemorrhage, at baseline is at an increased risk for ARIA. The incidence of brain hemorrhage and the size of a hemorrhage can be measured by tools known in the art and may include those described herein. In some embodiments, brain hemorrhage is measured by MRI. In some embodiments, the brain hemorrhage is measured by number of hemorrhages. In some embodiments, the brain hemorrhage is measured by the size of hemorrhage. In some embodiments, a microhemorrhage is a brain hemorrhage less than 1 cm in diameter as measured on radiographic imaging. In some embodiments, an intracerebral hemorrhage is a brain hemorrhage greater than 1 cm in diameter as measured on radiographic imaging. In some embodiments, a patient is monitored for brain hemorrhage prior to treatment, e.g., treatment with an anti-Aβ protofibril antibody, e.g., treatment with BAN2401, by radiographic imaging (e.g., MRI). In some embodiments, a patient with a microhemorrhage or intracerebral hemorrhage at baseline treated with an anti-Aβ protofibril antibody such as BAN2401 is administered a steroid. In some embodiments, a patient is monitored for brain hemorrhage at least once after treatment, e.g., treatment with an anti-Aβ protofibril antibody, e.g., treatment with BAN2401, by radiographic imaging (e.g., MRI). In some embodiments, a patient is monitored for brain hemorrhage more than once after treatment, e.g., treatment with an anti-Aβ protofibril antibody, e.g., treatment with BAN2401, by radiographic imaging (e.g., MRI). In some embodiments, the patient may be monitored after one or more administrations of an anti-Aβ protofibril antibody (e.g., BAN2401), for example, after 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, or more administrations. In some embodiments, the treatment may be continued if the clinical symptom severity and the radiographic severity are asymptomatic or mild. In some embodiments, e.g., if the treatment may be suspended and/or discontinued if the clinical symptom severity and/or the radiographic severity are moderate or severe. In some embodiments, a patient is monitored for brain hemorrhage at least once after the discontinuation of treatment. In some embodiments, a patient is monitored for brain hemorrhage at Attorney Docket No.08061.0062-00304 least 1 week, 2 weeks, 3 weeks, 1 month, 2 months, 3 months, 6 months, 12 month, 18 months, or 24 months after treatment discontinuation. In some embodiments, a patient with a microhemorrhage or intracerebral hemorrhage at baseline is not treated with an anti-Aβ protofibril antibody such as BAN2401. In some embodiments, a patient that does not present a microhemorrhage or intracerebral hemorrhage at baseline is treated with an anti-Aβ protofibril antibody such as BAN2401. In some embodiments, a patient with a microhemorrhage or intracerebral hemorrhage at baseline treated with an anti-Aβ protofibril antibody, such as BAN2401, is monitored more frequently, e.g., monitored for ARIA, than a patient without a microhemorrhage or intracerebral hemorrhage at baseline. In some embodiments, a patient that presents with CAA at baseline is not treated with an anti-Aβ protofibril antibody such as BAN2401. In some embodiments, treatment is discontinued in a patient who develops CAA. 4. Measurement of Brain White Matter The baseline status of a patient’s white matter in the brain and changes to a subject’s white matter can be measured by tools known in the art and may include those described herein. In some embodiments, the patient’s white matter is assessed by MRI. In some embodiments, the thickness of a patient’s white matter is assessed prior to treatment, e.g., treatment with an anti-Aβ protofibril antibody, e.g., treatment with BAN2401, by radiographic imaging (e.g., MRI). In some embodiments, a patient with a change in white matter from baseline, e.g., a decrease in white matter thickness, has an increased risk of ARIA with treatment with an anti-Aβ protofibril antibody, e.g., treatment with BAN2401. In some embodiments, a patient’s white matter is monitored for changes at least once after treatment, e.g., treatment with an anti-Aβ protofibril antibody, e.g., treatment with BAN2401, by radiographic imaging (e.g., MRI). In some embodiments, a patient’s white matter is monitored more than once after treatment, e.g., treatment with an anti-Aβ protofibril antibody, e.g., treatment with BAN2401, by radiographic imaging (e.g., MRI). In some embodiments, the patient may be monitored after one or more administrations of an anti-Aβ protofibril antibody (e.g., BAN2401), for example, after 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, or more administrations. In some embodiments, the treatment may be continued if the clinical symptom severity and the radiographic severity are asymptomatic or mild. In some embodiments, e.g., if the treatment may be suspended and/or discontinued if the clinical symptom severity and/or the radiographic severity are moderate or severe. In some embodiments, a patient is monitored for changes in white matter at least once after the discontinuation of treatment. In some embodiments, a patient is monitored for changes in white matter at least 1 week, 2 weeks, 3 weeks, 1 month, 2 months, 3 months, 6 months, 12 month, 18 months, or 24 months after treatment discontinuation. In some embodiments, a subject that has a change or decrease in brain white matter, e.g., as measured by brain imaging relative to baseline, is Attorney Docket No.08061.0062-00304 not selected for treatment with an anti-Aβ protofibril antibody (e.g., BAN2401). In some embodiments, a subject who does not have a decrease in brain white matter, e.g., as measured by brain imaging, prior to treatment is selected for treatment with an anti-Aβ protofibril antibody (e.g., BAN2401). 5. Selection of patient based on brain hemorrhage and/or brain white matter In some embodiments, a subject’s baseline microhemorrhage or intracerebral hemorrhage status may increase the risk of an ARIA event, intracerebral or microhemorrhage event after administration of an anti-Aβ protofibril antibody (e.g., BAN2401). In some embodiments, a patient is selected for treated with an anti-Aβ protofibril antibody such as BAN2401 if that patient has not had or does not currently have an ARIA event and/or intracerebral hemorrhage or microhemorrhage prior to treatment. In some embodiments, a subject who has had or currently has an intracerebral hemorrhage or a microhemorrhage at baseline is not selected for treatment with an anti-Aβ protofibril antibody, (e.g., BAN2401). In some embodiments, a subject exhibiting a change or decrease in brain white matter, e.g., as measured by brain imaging relative to baseline, is not selected for treatment with an anti-Aβ protofibril antibody (e.g., BAN2401). In some embodiments, a subject who has not exhibited a decrease in brain white matter, e.g., as measured by brain imaging, prior to treatment is selected for treatment with an anti-Aβ protofibril antibody (e.g., BAN2401). In some embodiments, a subject who has had or currently has an intracerebral hemorrhage or a microhemorrhage at baseline is selected for treatment with an anti-Aβ protofibril antibody, (e.g., BAN2401), and is monitored throughout the course of treatment for ARIA events, e.g., more frequently than a subject who has not exhibited a decrease in brain white matter. In some embodiments, a subject exhibiting a change or decrease in brain white matter, e.g., as measured by brain imaging relative to baseline, is selected for treatment with an anti-Aβ protofibril antibody (e.g., BAN2401), and is monitored throughout the course of treatment for ARIA events, e.g., more frequently than a subject who has not exhibited a decrease in brain white matter. In some embodiments, the subject exhibiting a change or decrease in brain white matter may be monitored prior to treatment with an anti-Aβ protofibril antibody (e.g., BAN2401), and prior to one or more infusions with the anti-Aβ protofibril antibody, e.g., prior to the fifth, seventh, and fourteenth infusions. In some embodiments, the subject may be continuously monitored during treatment. 6. Other risk factors for ARIA In some embodiments, other factors may affect a subject’s risk of ARIA when treated with an anti-Aβ protofibril antibody, e.g., treatment with BAN2401. A subject may be monitored for risk factors prior to or during administration of the anti-Aβ protofibril antibody. In Attorney Docket No.08061.0062-00304 some embodiments, a subject who is found to have a risk factor prior to treatment may be excluded or treated with an alternate therapy from an anti-Aβ protofibril antibody such as BAN2401. In some embodiments, a subject having a risk factor may begin treatment with the anti-Aβ protofibril antibody (e.g., BAN2401), but may be monitored for ARIA, e.g., monitored more frequently, during the treatment than a subject who does not have the risk factor. In some embodiments, ARIA may be monitored by radiographic imaging of the subject’s brain (e.g., by MRI). In some embodiments, the treatment may be discontinued if a subject is found to develop ARIA. In some embodiments, a subject who is not found to have a risk factor prior to treatment may be selected for treatment with an anti-Aβ protofibril antibody (e.g., BAN2401). In some embodiments, subjects who are carriers for the ApoE4 allele may have an increased risk of ARIA during treatment with an anti-Aβ protofibril antibody, e.g., treatment with BAN2401. Accordingly, in some embodiments, the subject’s ApoE4 status is assessed prior to treatment (e.g., treatment with an anti-Aβ protofibril antibody, e.g., treatment with BAN2401) by a DNA test of a body sample such as blood or a buccal swab. In some embodiments, a subject who is a carrier for the ApoE4 allele (e.g., either heterozygous or homozygous for the ApoE4 allele) may not be treated with an anti-Aβ protofibril antibody such as BAN2401. In some embodiments, a subject who is a carrier for the ApoE4 allele (e.g., either heterozygous or homozygous for the ApoE4 allele) may begin treatment with the anti-Aβ protofibril antibody (e.g., BAN2401), but may be monitored for ARIA more frequently during the treatment than a subject who is not a carrier for the ApoE4 allele. In some embodiments, treatment may be discontinued if a subject who is a carrier for the ApoE4 allele (e.g., either heterozygous or homozygous for the ApoE4 allele) is found to develop ARIA. In some embodiments, a subject who is not a carrier for the ApoE4 allele (e.g., either heterozygous or homozygous for the ApoE4 allele) is selected for treatment with an anti-Aβ protofibril antibody (e.g., BAN2401). In some embodiments, a subject with a higher blood pressure, also called higher mean arterial pressure (e.g., prior to and/or during treatment), as compared to a control (e.g., a blood pressure in a healthy subject or a threshold blood pressure measurement based on a population average), may have increased risk of ARIA when treated with an anti-Aβ protofibril antibody, e.g., treatment with BAN2401. In some embodiments, the subject’s mean arterial blood pressure is assessed prior to treatment (e.g., treatment with an anti-Aβ protofibril antibody, e.g., treatment with BAN2401), e.g., by auscultation, by measuring oscillations in blood flow and calculating blood flow, or measuring blood pressure with an invasive probe inserted directly into the lumen of an artery. In some embodiments, a subject who has a higher mean arterial pressure as compared to a control (e.g., a healthy subject) may not be treated with an anti-Aβ protofibril antibody such as BAN2401. In some embodiments, a high mean arterial pressure may be 130-139 mmHg/80-89 mmHg or higher. In some embodiments, a high mean arterial pressure may be 140 mmHg/90 mmHg or higher. In some Attorney Docket No.08061.0062-00304 embodiments, a high mean arterial pressure may be 180 mmHg/120 mmHg or higher. In some embodiments, a subject who has a higher mean arterial pressure as compared to a control may begin treatment with the anti-Aβ protofibril antibody (e.g., BAN2401), but may be monitored for ARIA more frequently during the treatment than a subject who does not have a higher mean arterial pressure as compared to a control. In some embodiments, the treatment may be discontinued if a subject’s blood pressure increases during treatment and/or the subject with higher mean arterial pressure is found to develop ARIA. In some embodiments, a subject who does not have higher mean arterial pressure is selected for treatment with an anti-Aβ protofibril antibody (e.g., BAN2401). In some embodiments, a subject with a greater amyloid burden (e.g., as determined by amyloid PET, or by a fluid biomarker such as an Aβ 42/40 ratio, e.g., measured prior to and/or during treatment), as compared to a control (e.g., a healthy subject), may have increased risk of ARIA when treated with an anti-Aβ protofibril antibody, e.g., treatment with BAN2401. In some embodiments, the subject’s amyloid burden is assessed prior to treatment (e.g., treatment with an anti- Aβ protofibril antibody, e.g., treatment with BAN2401), e.g., by PET imaging for amyloid PET, or by detection of a a fluid biomarker such as an Aβ 42/40 ratio. In some embodiments, a subject who has a higher amyloid burden as compared to a control (e.g., a healthy subject) may not be treated with an anti-Aβ protofibril antibody such as BAN2401. In some embodiments, a subject who has a higher amyloid burden as compared to a control may begin treatment with the anti-Aβ protofibril antibody (e.g., BAN2401), but may be monitored for ARIA more frequently during the treatment than a subject who does not have a higher amyloid burden as compared to a control. In some embodiments, the treatment may be discontinued if a subject develops a higher amyloid burden and/or the subject with a higher amyloid burden is found to develop ARIA. In some embodiments, a subject who does not have higher amyloid burden is selected for treatment with an anti-Aβ protofibril antibody (e.g., BAN2401). In some embodiments, a subject with cortical superficial siderosis (e.g., prior to and/or during treatment) may have increased risk of ARIA-E when treated with an anti-Aβ protofibril antibody, e.g., treatment with BAN2401. In some embodiments, the subject’s brain is scanned for superficial siderosis assessed prior to treatment (e.g., treatment with an anti-Aβ protofibril antibody, e.g., treatment with BAN2401), e.g., by imaging (e.g., by MRI). In some embodiments, a subject who has cortical superficial siderosis may not be treated with an anti-Aβ protofibril antibody such as BAN2401. In some embodiments, a subject who has cortical superficial siderosis may begin treatment with the anti-Aβ protofibril antibody (e.g., BAN2401), but may be monitored for ARIA more frequently during the treatment than a subject who does not have cortical superficial siderosis. In some embodiments, the treatment may be discontinued if a subject develops cortical superficial siderosis and/or the subject with cortical superficial siderosis is found to develop ARIA-E. In some embodiments, a subject who does not have cortical superficial siderosis is selected for treatment with an anti-Aβ protofibril antibody (e.g., BAN2401). Attorney Docket No.08061.0062-00304 7. Steroid use in treating severe ARIA In some embodiments, a patient with an increased risk of an intracerebral hemorrhage or microhemorrhage event and/or ARIA is administered a steroid before and/or during treatment with an anti-Aβ protofibril antibody such as BAN2401. In some embodiments, a patient exhibiting severe ARIA during treatment with an anti-Aβ protofibril antibody (e.g., BAN2401) is administered a steroid. Steroid treatment may be by any known route, e.g., intravenous and/or oral. Steroid dose and regimen may be according to those known in the art. In some embodiments, a patient with a severe radiographic or symptomatic ARIA-E is administered a steroid at a dose and/or frequency consistent with the standard of care known by one of ordinary skill in the art. 8. Use with anticoagulants, antiplatelet agents, and thrombolytic agents Without being bound by theory, it has been surprisingly found that patients concurrently administered certain anticoagulant or thrombolytic agents may have an equal or reduced risk of an ARIA event, cerebral hemorrhage, or microhemorrhage to a subject administered an anti-Aβ protofibril antibody such as BAN2401 alone. Again, without being bound by theory, some patients on certain anticoagulant or thrombolytic agents may have improved therapeutic outcomes when administered an anti-Aβ protofibril antibody such as BAN2401. In some embodiments, an AD subject or early AD subject is administered or treated with an anticoagulant or thrombolytic (e.g., aspirin, antiplatelet, anticoagulant, fibrinolytic, tissue plasminogen activator) medication. As used herein, a thrombolytic and an antithrombotic are used interchangeably. In some embodiments, the thrombolytic agent is aspirin. In some embodiments, the thrombolytic agent is an antiplatelet. In some embodiments, the thrombolytic agent is an anticoagulant. In some embodiments, the thrombolytic agent is a fibrinolytic agent. In some embodiments, the thrombolytic agent is a tissue plasminogen activator. In some embodiments, a subject treated with an anticoagulant medication is administered an anti-Aβ protofibril antibody such as BAN2401. In some embodiments, a subject treated with an anticoagulant medication and administered an anti-Aβ protofibril antibody such as BAN2401 is at an equal or reduced risk of an ARIA event or intracerebral hemorrhage as compared to a subject administered an anti-Aβ protofibril antibody such as BAN2401 alone. In some embodiments, a subject treated with an antiplatelet medication is administered an anti-Aβ protofibril antibody such as BAN2401. In some embodiments, a subject treated with an antiplatelet medication and administered an anti-Aβ protofibril antibody such as BAN2401 is at an equal or reduced risk of an ARIA event or intracerebral hemorrhage as compared to a subject administered an anti-Aβ protofibril antibody such as BAN2401 alone. In some embodiments, a subject treated with aspirin is administered an anti-Aβ protofibril antibody such as BAN2401. In some embodiments, a subject treated with aspirin and administered an anti-Aβ protofibril antibody such as BAN2401 is at an equal or reduced risk of an ARIA event or intracerebral Attorney Docket No.08061.0062-00304 hemorrhage as compared to a subject administered an anti-Aβ protofibril antibody such as BAN2401 alone. In some embodiments, a subject receiving the anti-Aβ protofibril antibody such as BAN2401 is not administered an anticoagulant or a thrombolytic agent. In some embodiments, a subject treated with an anticoagulant or a thrombolytic agent is not selected for treatment with an anti-Aβ protofibril antibody such as BAN2401. In some embodiments, the patient receiving the anti-Aβ protofibril antibody such as BAN2401 is not administered a tissue plasminogen activator. In some embodiments, a subject treated with a tissue plasminogen activator is not selected for treatment with an anti-Aβ protofibril antibody such as BAN2401. In some embodiments a patient treated with a tissue plasminogen activator is administered an anti-Aβ protofibril antibody such as BAN2401, e.g., with additional monitoring for ARIA. In some embodiments, the patient receiving the anti-Aβ protofibril antibody such as BAN2401 that is also receiving an anticoagulant or a thrombolytic agent is monitored for an ARIA event. In some embodiments, the patient receiving the anti-Aβ protofibril antibody such as BAN2401 that is also receiving an anticoagulant or a thrombolytic agent will stop receiving the anti-Aβ protofibril antibody until treatment with the anticoagulant or thrombolytic agent is discontinued. In some embodiments, a subject’s brain may be monitored (e.g., by MRI) at any time during treatment with the anti-Aβ protofibril antibody such as BAN2401. Extra monitoring may be performed, for example, when the subject has factors that indicate an increased risk for intracerebral hemorrhage, such as subjects who are on anticoagulant therapy. In some embodiments, a subject who is administered a steroid may be monitored further, e.g., by MRI. 9. Selection of patient and monitoring for change in regimen based on biomarkers a. Measurement of Tau PET The disclosure and methods discussed herein turn in part on the discovery that biomarker, such as a tau PET level, can be used to select a patient for treatment, to allow for monitoring and treatment decisions such as whether to increase or decrease the amount of antibody being administered, determine whether to increase or decrease the frequency of administration, determine whether to introduce a further therapeutic agent, determine whether to switch to a maintenance dose, and/or whether to discontinue treatment with the anti-Aβ protofibril antibody, alone or in combination of other biomarkers. A treatment comprising an anti-Aβ protofibril antibody such as BAN2401 can lead to a reduced rate of tau accumulation, as measured by a tau PET level (e.g., as measured by tau PET imaging), e.g., in a brain region such as a temporal region, as compared to a control patient. In some embodiments, this correlates with reduced brain amyloid load and improved cognitive outcomes in subjects. Without being bound by theory, a tau PET level (e.g., a tau PET standard uptake value ratio (SUVr)) may be used, in various embodiments, as a less invasive and/or additional biomarker for Attorney Docket No.08061.0062-00304 refining the measurement of treatment efficacy and/or to allow for monitoring and treatment decisions. Such decision may include whether to increase or decrease the amount of an anti-Aβ protofibril antibody being administered, whether to increase or decrease the frequency of administration, whether to introduce a further therapeutic agent, and/or whether to discontinue treatment with the anti-Aβ protofibril antibody. As used herein, the term “tau PET” refers to tau positron emission tomography imaging. In some embodiments, tau PET imaging (also referred to as a PET scan) is performed to assess for tau pathology. In some embodiments, tau PET is assessed with a PET tracer and uses the same tracer in follow-up assessments. In some embodiments, the PET imaging uses a [18F]MK-6240tracer. Tau positron emission tomography (PET) imaging can be used to confirm the presence of tau pathology in the brain of early AD subjects in the screening phase of the study and/or to evaluate the effects of the at least one anti-Aβ protofibril antibody on amyloid levels in the brain, both by whole brain analysis (e.g., the average of 5-6 cortical regions) and brain region analysis (e.g., in a temporal brain region). In some embodiments, the PET scan uses a [18F]MK-6240 (florquinitau) tracer. In some embodiments, tau load can be identified by a PET imaging uptake visual read, e.g., by a trained radiologist. In embodiments, regions of the brain are assessed for uptake of the imaging agent. In some embodiments, the temporal region is assessed for a tau PET level. In some embodiments, the frontal region is assessed for a tau PET level. In some embodiments, the parietal region is assessed for a tau PET level. In some embodiments, the occipital region is assessed for a tau PET level. In some embodiments, the cingulate region is assessed for a tau PET level. In some embodiments, the temporal region comprises the medial temporal region. In some embodiments, the medial temporal region comprises the hippocampus, the entorhinal cortex, the parahippocampus, and/or the anterior medial/lateral temporal lobes. In some embodiments, the temporal region comprises the meta-temporal region. In some embodiments, the meta-temporal region comprises the amygdala, the entorhinal cortex, the parahippocampus, the middle/interior and posterior temporal lobe, and/or the fusiform region. In some embodiments, the temporal region comprises the temporal lobe. In some embodiments, the temporal lobe comprises the superior anterior/posterior temporal lobe, the middle/inferior temporal lobe, the posterior temporal lobe, and/or the fusiform cortex. In some embodiments, the whole cortical gray matter is assessed for a tau PET level. In some embodiments, the reference region used for assessing a tau PET level is the ventral cerebellum (Cb). In some embodiments, a “tau PET level” can be identified by a standard uptake value ratio (SUVr) as compared to a reference region as measured by tau PET imaging. As used herein, a “tau PET level”, “tau level in a brain” and “tau load” are used interchangeably. As used herein a tau PET level refers to a measurement of a level of tau in a brain region, e.g., a temporal region, by PET. Methods for calculating tau PET SUVr are known in the art and may include those described herein. Attorney Docket No.08061.0062-00304 In some embodiments, a Standard Uptake Value Ratio Quantitative analysis of amyloid levels is completed using PMOD PNEURO Biomedical Image Quantification Software (PMOD Technologies, Zurich, Switzerland). In some embodiments, PET images are first assessed for subject movement in the X, Y, and Z planes and corrected for motion, if needed, before individual images (e.g., 5-minute emission frames) are averaged, e.g., using a PMOD Averaging Function (PET frames averaged to increase the signal to noise ratio). In some embodiments, corresponding MRIs from subjects are prepared (e.g., using matrix size reduction processing, cropping of the MRI to include only the brain, segmentation to separate images into binary maps of gray matter, white matter, and CSF, and stripping the image of skull leaving only brain mask). In some embodiments, the averaged PET images and prepared MRIs are matched using the PMOD Matching Function, placing the images in the same orientation. In some embodiments, a Brain Normalization function, e.g., as provided by PMOD software, is used along with Brain Norm and Rigid Matching transformation matrices, to produce an averaged PET. In some embodiments, this averaged PET which is normalized to the MNInst space (Senjem et al, 2005) that is in the same orientation as the subject’s segmented MRI for quantitative analysis. In some embodiments, the PMOD Mask Function is used to mask the brain and zero the image outside of the mask to create a Normalized Gray Matter PET and a Normalized White Matter PET. Standard uptake values (SUVs) may be calculated for all gray matter mapped regions and the 3 white matter regions (pons, cerebellar white, and subcortical white) using PMOD software calculated using the normalized PET, subject weight, and injected dose of tracer to arrive at the units of SUVs. In some embodiments, the SUVr is the ratio of the global cortical average as compared to a reference region of choice. In some embodiments, a whole cerebellum mask is used as the reference region. In some embodiments, the reference region is subcortical white matter, ventral cerebellum, derived whole cerebellum, whole cerebellum adjusted by subcortical white matter, cerebellar gray matter, and composite reference regions consisting of cerebellar cortex, pons subcortical white matter, and cerebella white matter. In some embodiments, the adjusted mean change from baseline is measured prior to treatment and at least once after the start of treatment, e.g., over a period of at least 6 months after an initial dose of a treatment. In some embodiments, the adjusted mean change from baseline is measured over a period of at least 12 months after an initial dose of a treatment. In some embodiments, the adjusted mean change from baseline is measured over a period of at least 13 months after an initial dose of a treatment. In some embodiments, the adjusted mean change from baseline is measured over a period of at least 18 months after an initial dose of a treatment. In some embodiments, after administration of the first dose of the composition the adjusted mean change from baseline in a subject’s tau PET SUVr value is less than 0.15. In some embodiments, after administration of the first dose of the composition the adjusted mean change from baseline in a subject’s tau PET SUVr value is less than 0.10. In some embodiments, after administration of the first Attorney Docket No.08061.0062-00304 dose of the composition the adjusted mean change from baseline in a subject’s tau PET SUVr value is less than 0.05. In some embodiments, 13 months after an initial dose of a treatment, the adjusted mean change from baseline in a subject’s tau PET SUVr value is less than 0.15. In some embodiments, after administration of the first dose of the composition the adjusted mean change from baseline in a subject’s tau PET SUVr value is less than 0.05. In some embodiments, 18 months after an initial dose of a treatment, the adjusted mean change from baseline in a subject’s tau PET SUVr value is less than 0.15. Additional methods for measuring tau by positron emission tomography (PET) are known in the art. Methods may include the Tau^IQ algorithm (see, e.g., Whittington et al., J. Nucl Med.2021 Sep 1;62(9):1292-1300 for quantitatively measuring tau PET radiotracers). The measurement of a tau PET level may be used alone to evaluate treatment efficacy, or in conjunction with one or more additional criteria, such as one or more measurement in a biofluid (e.g., p-tau181 and/or a ratio of Aβ1-42 to Aβ1-40), PET measurement of Aβ (e.g., via radiotracer uptake), MRI evaluation of Aβ plaque, and/or behavioral measures, as discussed herein. Such assays may also be used to diagnose patients eligible for treatment (e.g. by measuring a tau PET level and determining a subject is suitable for treatment because of a higher tau PET level than observed in a healthy control subject, alone or in conjunction with measuring one or more additional marker of AD pathology in the subject).In some embodiments, a subject is selected for treatment because of a high tau PET level in a region of the brain of the subject, wherein the tau PET level is greater than a subject who does not have AD. In some embodiments, a subject is selected for treatment because of a high tau PET level in the temporal region of the brain of the subject, wherein the tau PET level is greater than 1.4 as measured by amyloid PET SUVr. In some embodiments, a subject is selected for treatment because of a high tau PET level in the temporal region of the brain of the subject, wherein the tau PET level is greater than 1.5 as measured by amyloid PET SUVr. In some embodiments, the measurement of a tau PET level may be used in place of another method of measuring brain tau levels and/or in place of another marker of Aβ. In some embodiments, the measurement of a tau PET level may be used in conjunction with measuring one or more additional markers. In some embodiments, a patient may be monitored by one or more additional biomarkers such as, but not limited to: (a) tau detected by PET scan from either a visual read or semiquantitative thresholds (SUVr or centiloid); (b) cerebrospinal fluid (CSF) total tau (t-tau); and/or (c) blood biomarkers (such as plasma total tau (T- tau), and/or phosphorylated tau (P-tau)(e.g., p-tau181)). In some embodiments, a patient’s tau PET level may be monitored in conjunction with one or more of a ratio of Aβ1-42 to Aβ1-40 and/or a p- tau181 measurements in a fluid sample, e.g., a blood sample. In some embodiments, the combination comprises a serum or plasma GFAP measurement. In some embodiments, the measurement of a tau PET level may be used in place of another method of measuring brain tau levels for determining Attorney Docket No.08061.0062-00304 treatment efficacy and/or making treatment decisions such as whether to continue treatment, switch to a maintenance dose, etc. In some embodiments, a tau PET level may be used to calculate a relative change from a baseline measurement (e.g., a measurement of a tau PET level before beginning a treatment). In some embodiments, a tau PET level measurement may be repeated after the start of a treatment regimen to monitor treatment efficacy. In some embodiments, a tau PET level that increased by no more than 0.05-0.1 over a 13-month period in a region of the brain indicates treatment efficacy. In some embodiments, a tau PET level that increased by no more than 0.05-0.1 over an 18-month period in a region of the brain indicates treatment efficacy. In some embodiments, a tau PET level that increased by no more than 0.05-0.1 over a 13-month period in the temporal region of the brain indicates treatment efficacy. In some embodiments, a tau PET level that increased by no more than 0.05-0.1 over an 18-month period in the temporal region of the brain indicates treatment efficacy. In some embodiments, a rate of change of a tau PET level is calculated based on two measurements from a subject. In some embodiments, a rate of change of a tau PET level is calculated based on more than two measurements from a subject. In some embodiments, a rate of change of a tau PET level indicates the rate of tau accumulation in the brain of a subject. In some embodiments, a rate of change of a tau PET level is calculated based on at least two measurements from a subject, wherein one measurement is taken from a subject before a treatment, and a second measurement is taken after the start of treatment, wherein treatment continues for at least 13 or 18 months after an initial dose of a treatment. In some embodiments, the rate of change of the tau PET level is compared to the rate of change of the tau PET level in an untreated control subject who has AD and has not received treatment. In some embodiments, a lower rate of tau PET increase relative to an untreated control subject indicates treatment efficacy. In some embodiments, a lower rate of tau PET increase over a 6-month period relative to an untreated control subject indicates treatment efficacy. In some embodiments, a lower rate of tau PET increase over a 12-month period relative to an untreated control subject indicates treatment efficacy. In some embodiments, a lower rate of tau PET increase over a 13-month period relative to an untreated control subject indicates treatment efficacy. In some embodiments, a lower rate of tau PET increase over an 18-month period relative to an untreated control subject indicates treatment efficacy. Methods of measuring clinical efficacy or monitoring a treatment may employ a set threshold to determine a change in brain tau levels, e.g., to identify a patient suitable for treatment, e.g., with an anti-Aβ protofibril antibody, or to determine whether to continue treatment, or to determine whether to switch to a maintenance dose, or to conclude a patient is amyloid negative. In some embodiments, the tau PET level threshold may be evaluated in conjunction with another measurement of brain amyloid load, such as an amyloid PET scan, a CSF or serum or plasma Attorney Docket No.08061.0062-00304 biomarker, to assist in determining whether a subject is suitable for treatment or continued treatment. In some embodiments, a tau PET level may be used in place of another method of measuring brain tau levels. In some embodiments, a tau PET level greater than a threshold level is used to determine if a patient is suitable for treatment. In some embodiments, a tau PET level threshold is about 1.4. In some embodiments, a tau PET level threshold is about 1.5. In some embodiments, a subject is selected for treatment with an anti-amyloid β (Aβ) protofibril antibody, wherein the subject has a tau PET level in a region of the brain greater than about 1.4. In some embodiments, a subject is selected for treatment with an anti-amyloid β (Aβ) protofibril antibody, wherein the subject has a tau PET level in a region of the brain greater than about 1.5. In some embodiments, the region of the brain is the temporal region. In some embodiments, the region of the brain is the temporal lobe. In some embodiments, the region of the brain is the meta-temporal lobe. In some embodiments, the region of the brain is the medial-temporal lobe. b. Measurement of Aβ42/40 ratio The disclosure and methods discussed herein depend in part on the discovery that a biomarker, such as an Aβ42/40 ratio, can be used to select a patient for treatment, to allow for monitoring and treatment decisions such as whether to increase or decrease the amount of antibody being administered, determine whether to increase or decrease the frequency of administration, determine whether to introduce a further therapeutic agent, determine whether to switch to a maintenance dose, and/or whether to discontinue treatment with the anti-Aβ protofibril antibody, alone or in combination of other biomarkers. Aβ42 and 40 be measured to calculate a ratio in blood samples, as disclosed in PCT/US2022/073576, which herein is incorporated by reference. A treatment comprising an anti-Aβ protofibril antibody such as BAN2401 can lead to an increase in the Aβ42/40 ratio that correlates with reduced brain amyloid load and improved cognitive outcomes in subjects. Methods for measuring the Aβ42/40 ratio are known in the art, such as assays using LC MS/MS. Methods may include the PrecivityAD^TM assay (see, e.g., Kirmess et al., J. Clinica Chimica Acta 519: 267-275 (2021)) and the Sysmex assay (https://www.eisai.com/news/2019/news201990.html) for measuring Aβ42 and Aβ40 in a sample to use in calculating a ratio. The measurement of the Aβ42/40 ratio may be used alone to evaluate treatment efficacy, or in conjunction with one or more additional criteria, such as a tau PET level, a PET measurement of Aβ radiotracer update, MRI evaluation of Aβ plaque, and/or behavioral measures, as discussed herein. Such assays may also be used to diagnose patients eligible for treatment (e.g. by measuring an Aβ42/40 ratio and determining a subject is suitable for treatment because of a lower ratio than observed in a healthy control subject, alone or in conjunction with measuring one or more additional marker of AD pathology in the subject). In some embodiments, the measurement of an Aβ42/40 ratio Attorney Docket No.08061.0062-00304 may be used in place of another method of measuring brain amyloid levels, such as a PET scan for determining a subject is suitable for treatment. In some embodiments, the measurement of an Aβ42/40 ratio may be used in place of another method of measuring brain amyloid levels, such as a PET scan for determining treatment efficacy and/or making treatment decisions such as whether to continue treatment, switch to a maintenance dose, etc. In some embodiments, an Aβ42/40 ratio measurement may employ a relative change from baseline measurement. In some embodiments, an Aβ42/40 ratio measurement may employ a set threshold to determine a change in brain amyloid levels, e.g., to identify a patient suitable for treatment, e.g., with an anti-Aβ protofibril antibody, or to determine whether to continue treatment, or to determine whether to switch to a maintenance dose, or to conclude a patient is amyloid negative. In some embodiments, the threshold may be evaluated in conjunction with another measurement of brain amyloid load, such as a PET scan, to assist in determining whether a subject is suitable for treatment or continued treatment. In some embodiments, an Aβ42/40 ratio threshold may be used in place of another method of measuring brain amyloid levels, such as a PET scan, to determine amyloid positivity. In some embodiments, an Aβ42/40 ratio threshold is at or about 0.09, 0.091, 0.092, 0.093, 0.094, 0.095, 0.096, 0.097, 0.099, 0.1. In some embodiments, the threshold is about 0.092. In some embodiments, the threshold is 0.092. In some embodiments, the threshold is about 0.094. In some embodiments, a decrease in the Aβ42/40 ratio below a threshold value may indicate a need to continue treatment or to select an increase in a dosing regimen. In some embodiments, an increase in the Aβ42/40 ratio above a threshold value may be used to indicate a treatment may be terminated (e.g., terminated in favor of a maintenance regimen) and/or to otherwise to determine a decrease in a dosing regimen or discontinuation in treatment. In some embodiments, a decrease in the Aβ42/40 ratio below a threshold value may be used to determine whether to discontinue a maintenance dosing regimen, e.g., and return to the prior treatment regimen. c. Measurement of a p-tau level The disclosure and methods discussed herein depend in part on the discovery that a biomarker, such as a p-tau level, can be used to select a patient for treatment, to allow for monitoring and treatment decisions such as whether to increase or decrease the amount of antibody being administered, determine whether to increase or decrease the frequency of administration, determine whether to introduce a further therapeutic agent, determine whether to switch to a maintenance dose, and/or whether to discontinue treatment with the anti-Aβ protofibril antibody, but also in combination of other biomarkers, such as a phosphorylated tau (p-tau) level, including tau phosphorylated at 181 (P-tau181), 217 (P-tau217), and/or 231 (P-tau231), and/or the ratio of P-tau181/NP-tau181, and/or the ratio of P-tau217/NP-tau217). A p-tau level can be measured in CSF, serum, or plasma, as disclosed in PCT/US2022/079571, which herein is incorporated by reference. A treatment comprising an anti- Attorney Docket No.08061.0062-00304 Aβ protofibril antibody such as BAN2401 can lead to a decrease in a p-tau181 level that correlates with reduced brain amyloid load and improved cognitive outcomes in subjects. Methods for measuring p-tau ratio are known in the art, such as immunoassay (e.g., a Quanterix™ Simoa^® p-tau assay) and/or mass spectrophotometry (IP/LC-MS/MS) based technology methods. Plasma p-tau181 is elevated in early stages of AD as determined by Braak staging (I-II) and continues to increase as the disease progresses into Braak stage V-VI (Janelidze et al., “Plasma P- tau181 in Alzheimer's disease: relationship to other biomarkers, differential diagnosis, neuropathology and longitudinal progression to Alzheimer's dementia,” Nat. Med., 26(3):379-386 (2020)). The biomarker highly correlates with amyloid PET and Tau PET and has demonstrated a 3.5-fold elevation in AD compared to control, with an intermediate increase in the MCI group, and appears to differentiate patients with clinically diagnosed AD from other tauopathies as well (Thijssen et al., “Diagnostic value of plasma phosphorylated tau181 in Alzheimer's disease and frontotemporal lobar degeneration,” Nat. Med., 26(3):387-397 (2020); Janelidze et al.). The measurement of the p-tau level (e.g., a p-tau181 level, a p-tau217 level, and/or a p- tau231 level, and/or the ratio of p-tau181/np-tau181, and/or the ratio of p-tau217/np-tau217) may be used alone to evaluate treatment efficacy, or in conjunction with one or more additional criteria, such as a tau PET level, a PET measurement of Aβ radiotracer update, MRI evaluation of Aβ plaque, and/or behavioral measures, as discussed herein. Such assays may also be used to diagnose patients eligible for treatment (e.g. by measuring the level of p-tau (e.g., a p-tau181 level, a p-tau217 level, and/or a p-tau231 level, and/or the ratio of p-tau181/np-tau181, and/or the ratio of p-tau217/np- tau217) and determining a subject is suitable for treatment because of a higher level than observed in a healthy control subject, alone or in conjunction with measuring one or more additional marker of AD pathology in the subject). In some embodiments, the measurement of the level of p-tau (e.g., a p- tau181 level, a p-tau217 level, and/or a p-tau231 level, and/or the ratio of p-tau181/np-tau181, and/or the ratio of p-tau217/np-tau217) may be used in place of another method of measuring brain amyloid levels, such as a PET scan for determining a subject is suitable for treatment. In some embodiments, the measurement of the level of p-tau (e.g., a p-tau181 level, a p-tau217 level, and/or a p-tau231 level, and/or the ratio of p-tau181/np-tau181, and/or the ratio of p-tau217/np-tau217) may be used in place of another method of measuring brain amyloid levels, such as a PET scan for determining treatment efficacy and/or making treatment decisions such as whether to continue treatment, switch to a maintenance dose, etc. In some embodiments, a plasma or serum p-tau181 level measurement may employ a relative change from baseline measurement. In some embodiments, a change in the p-tau181 level may be used to evaluate treatment efficacy. In some embodiments, a decrease in the level of p-tau181 indicates treatment efficacy, e.g., a reduction in brain amyloid levels. In some embodiments, a p- Attorney Docket No.08061.0062-00304 tau181 level measurement may employ a set threshold to determine a change in brain amyloid levels, e.g., to identify and/or select a patient suitable for treatment, e.g., with an anti-Aβ protofibril antibody, or to determine whether to continue treatment, or to determine whether to switch to a maintenance dose, or to conclude a patient is amyloid negative. In some embodiments, the threshold may be evaluated in conjunction with another measurement of brain amyloid load, such as a PET scan, to assist in determining whether a subject is suitable for treatment or continued treatment. In some embodiments, a p-tau181 level threshold may be used in place of another method of measuring brain amyloid levels, such as a PET scan. In some embodiments, a p-tau181 level threshold at or above about 2.2 to 2.3 pg/mL is used to identify and/or select a patient suitable for treatment, e.g., with an anti-Aβ protofibril antibody. In some embodiments, a p-tau181 level threshold at or above about 2.2 pg/mL is used to identify and/or select a patient suitable for treatment, e.g., with an anti-Aβ protofibril antibody. In some embodiments, a p-tau181 level threshold at or above about 2.3 pg/mL is used to identify and/or select a patient suitable for treatment, e.g., with an anti-Aβ protofibril antibody. In certain such embodiments, the p-tau181 level is measured using a Quanterix™ Simoa^® p-tau assay. In some embodiments, the threshold is about 2.3 pg/mL. In some embodiments, the threshold is about 2.2 pg/mL. In some embodiments, an increase in the p-tau181 level above a threshold value may indicate a need to continue treatment or to select an increase in a dosing regimen. In some embodiments, a decrease in the p-tau181 level below a threshold value may be used to indicate a treatment may be terminated (e.g., terminated in favor of a maintenance regimen) and/or to otherwise to determine a decrease in a dosing regimen or discontinuation in treatment. In some embodiments, p-tau 181 levels may be measured in the blood, e.g., where a blood- based test is faster, easier, and/or more cost effective than an assay of cerebrospinal fluid (CSF) or imaging methods. p-tau 181, in particular, has been shown to correlate with brain amyloid burden, tau accumulation, and clinical progression in pre-clinical and early AD individuals (Wang YL et al., Plasma p-tau181 Level Predicts Neurodegeneration and Progression to Alzheimer's Dementia: A Longitudinal Study. Front Neurol.4382021;12:695696.; Jack CR et al., Predicting amyloid PET and tau PET stages with plasma biomarkers. Brain.2023;146:2029-44). In some embodiments, a higher tau PET level (e.g., p-tau 181) in a subject as compared with a healthy control subject indicate that a subject with pre-AD or at risk for AD or with early AD will progress over the next 18 months and/or may predict 36-month progression from Aβ+ mild cognitive impairment to AD. d. Plasma or serum level of GFAP In some embodiments, administration of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein to a subject results in a reduction in glial fibrillary acidic protein (GFAP) in the plasma or serum of a subject. Without being bound by theory, the GFAP level may be used as a marker of astrocyte activation. The GFAP level Attorney Docket No.08061.0062-00304 may be measured by techniques known in the art, such as an immunoassay (e.g., a Quanterix™ Simoa® assay) and/or mass spectrophotometry (IP/LC-MS/MS) based technology methods. In some embodiments, administration of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein to a subject results in a reduction in plasma or serum levels of GFAP in the subject. In some embodiments, the administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction of at least 1%, at least 2%, at least 3%, at least 4%, at least 5%, at least 6%, at least 7%, at least 8%, at least 9%, or at least 10%, relative to baseline, in the plasma or serum level of GFAP. In some embodiments, a serum level of GFAP, may be used to select a patient for treatment, to allow for monitoring and treatment decisions such as whether to increase or decrease the amount of antibody being administered, determine whether to increase or decrease the frequency of administration, determine whether to introduce a further therapeutic agent, determine whether to switch to a maintenance dose, and/or whether to discontinue treatment with the anti-Aβ protofibril antibody. In some embodiments, additional biomarkers in combination with a decreasing GFAP level over the same period, may indicate an effective treatment. In some embodiments, improvements in other biomarkers in combination with a decreasing GFAP level over the same period, may indicate an effective treatment. In some embodiments, improvements in other biomarkers in combination with a decreased GFAP level relative to an untreated control, may indicate an effective treatment. In some embodiments, an indication of the efficacy of treatment may be used to decrease the amount of antibody being administered, decrease the frequency of administration, or to switch to a maintenance dose. e. Cerebrospinal Fluid Level of Neurogranin In some embodiments, administration of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein to a subject results in a reduction in cerebrospinal fluid level of neurogranin in the subject. In some embodiments, the administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction of at least 1%, at least 2%, at least 3%, at least 4%, at least 5%, at least 6%, at least 7%, at least 8%, at least 9%, or at least 10%, relative to baseline, in cerebrospinal fluid level of neurogranin. In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction in cerebrospinal fluid level of neurogranin after 18 months of administration of the composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody. In some embodiments, administration to a subject of a composition comprising a Attorney Docket No.08061.0062-00304 therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction of at least 1%, at least 2%, at least 3%, at least 4%, at least 5%, at least 6%, at least 7%, at least 8%, at least 9%, or at least 10%, relative to baseline, cerebrospinal fluid level of neurogranin after 18 months of administration of the composition. In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction of at least about 25 pg/mL, at least about 30 pg/mL, at least about 35 pg/mL, at least about 40 pg/mL, at least about 45 pg/mL, at least about 50 pg/mL, at least about 55 pg/mL, at least about 60 pg/mL, or at least about 65 pg/mL, relative to baseline, cerebrospinal fluid level of neurogranin. In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction of at least about 65 pg/mL, relative to baseline, cerebrospinal fluid level of neurogranin. In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction of at least about 25 pg/mL, at least about 30 pg/mL, at least about 35 pg/mL, at least about 40 pg/mL, at least about 45 pg/mL, at least about 50 pg/mL, at least about 55 pg/mL, at least about 60 pg/mL, or at least about 65 pg/mL, relative to baseline, of cerebrospinal fluid level of neurogranin after 18 months of administration of the composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody. In some embodiments, administering to a subject a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction of at least 65 pg/mL, relative to baseline, of cerebrospinal fluid level of neurogranin after 18 months of administration of the composition. In some embodiments, the at least one anti-Aβ protofibril antibody is BAN2401. In some embodiments, the therapeutically effective amount of at least one anti-Aβ protofibril antibody is 10 mg/kg. In some embodiments, the composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein is administered bi- weekly or monthly. In some embodiments, a composition comprising 10 mg/kg of BAN2401 is administered bi-weekly. In some embodiments, a composition comprising 10 mg/kg of BAN2401 is administered monthly. In some embodiments, a cerebrospinal fluid level of neurogranin, may be used to select a patient for treatment, to allow for monitoring and treatment decisions such as whether to increase or decrease the amount of antibody being administered, determine whether to increase or decrease the frequency of administration, determine whether to introduce a further therapeutic agent, determine whether to switch to a maintenance dose, and/or whether to discontinue treatment with the anti-Aβ protofibril antibody. In some embodiments, an improvement in an additional biomarker, in Attorney Docket No.08061.0062-00304 combination with a decreasing cerebrospinal fluid level of neurogranin over the same period, may indicate an effective treatment. In some embodiments, an improvement in an additional biomarker, in combination with a decreasing cerebrospinal fluid level of neurogranin over the same period, may indicate an effective treatment. In some embodiments, an improvement in an additional biomarker, in combination with a decreased cerebrospinal fluid level of neurogranin relative to an untreated control, may indicate an effective treatment. In some embodiments, an indication of the efficacy of treatment may be used to decrease the amount of antibody being administered, decrease the frequency of administration, or to switch to a maintenance dose. f. Level of Neurofilament Light Chain In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction, relative to placebo, in cerebrospinal fluid level and/or the plasma or serum level of neurofilament light chain. In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction of at least 5%, at least 10%, at least 15%, at least 20%, at least 25%, at least 30%, at least 35%, at least 40%, at least 45%, or at least 50%, relative to placebo, in cerebrospinal fluid level and/or the plasma or serum level of neurofilament light chain. In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction, relative to placebo, in cerebrospinal fluid level and/or the plasma or serum level of neurofilament light chain after 18 months of administration of the composition. In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction, relative to placebo, of at least 5%, at least 10%, at least 15%, at least 20%, at least 25%, at least 30%, at least 35%, at least 40%, at least 45%, or at least 50%, relative to baseline, in cerebrospinal fluid level and/or the plasma or serum level of neurofilament light chain after 18 months of administration of the composition. In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in production of more than about 35 pg/mL, about 40 pg/mL, about 45 pg/mL, about 50 pg/mL, about 55 pg/mL, about 60 pg/mL, about 65 pg/mL, about 70 pg/mL, about 75 pg/mL, relative to baseline, of cerebrospinal fluid level of neurofilament light chain. In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in production of no more than about 75 pg/mL, relative to baseline, of cerebrospinal fluid level of neurofilament light chain. Attorney Docket No.08061.0062-00304 In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in production of more than about 35 pg/mL, about 40 pg/mL, about 45 pg/mL, about 50 pg/mL, about 55 pg/mL, about 60 pg/mL, about 65 pg/mL, about 70 pg/mL, about 75 pg/mL, relative to baseline, of cerebrospinal fluid level of neurofilament light chain after 18 months of administration of the composition. In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in production of no more than about 75 pg/mL, relative to baseline, of cerebrospinal fluid level of neurofilament light chain after 18 months of administration of the composition. In some embodiments, the at least one anti-Aβ protofibril antibody is BAN2401. In some embodiments, the therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein is 10 mg/kg. In some embodiments, a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein is administered bi-weekly or monthly. In some embodiments, a composition comprising 10 mg/kg of BAN2401 is administered bi-weekly. In some embodiments, a composition comprising 10 mg/kg of BAN2401 is administered monthly. In some embodiments, an additional biomarker and a plasma or serum level of neurofilament light, may be used to select a patient for treatment, to allow for monitoring and treatment decisions such as whether to increase or decrease the amount of antibody being administered, determine whether to increase or decrease the frequency of administration, determine whether to introduce a further therapeutic agent, determine whether to switch to a maintenance dose, and/or whether to discontinue treatment with the anti-Aβ protofibril antibody. In some embodiments, an improvement in an additional biomarker, in combination with a decreasing plasma or serum level of neurofilament light over the same period, may indicate an effective treatment. In some embodiments, an improvement in an additional biomarker, in combination with a decreasing plasma or serum level of neurofilament light over the same period, may indicate an effective treatment. In some embodiments, an improvement in an additional biomarker, t in combination with a decreased plasma or serum level of neurofilament light relative to an untreated control, may indicate an effective treatment. In some embodiments, an indication of the efficacy of treatment may be used to decrease the amount of antibody being administered, decrease the frequency of administration, or to switch to a maintenance dose. g. Cerebrospinal Fluid Level of Phospho-Tau In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction in cerebrospinal fluid level of phospho-Tau (p-tau). In some embodiments, administration Attorney Docket No.08061.0062-00304 to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction of at least 1%, at least 2%, at least 3%, at least 4%, at least 5%, at least 6%, at least 7%, at least 8%, at least 9%, at least 10%, at least 11%, at least 12%, or at least 13% relative to baseline, of cerebrospinal fluid level of phospho-Tau. In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction in cerebrospinal fluid level of phospho-Tau after 18 months of administration of the composition. In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction of at least 1%, at least 2%, at least 3%, at least 4%, at least 5%, at least 6%, at least 7%, at least 8%, at least 9%, at least 10%, at least 11%, at least 12%, or at least 13%, relative to baseline, of cerebrospinal fluid level of phospho-Tau after 18 months of administration of the composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody. In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction of at least about 65 pg/mL, at least about 70 pg/mL, at least about 75 pg/mL, at least about 80 pg/mL, at least about 85 pg/mL, at least about 90 pg/mL, or at least about 95 pg/mL, relative to baseline, of cerebrospinal fluid level of phospho-Tau. In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction of at least about 95 pg/mL, relative to baseline, of cerebrospinal fluid level of phospho-Tau. In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction of at least about 65 pg/mL, at least about 70 pg/mL, at least about 75 pg/mL, at least about 80 pg/mL, at least about 85 pg/mL, at least about 90 pg/mL, or at least about 95 pg/mL, relative to baseline, of cerebrospinal fluid level of phospho-Tau after 18 months of administration of the composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody. In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in a reduction of at least 95 pg/mL, relative to baseline, of cerebrospinal fluid level of phospho-Tau after 18 months of administration of the composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody. In some embodiments, the at least one anti-Aβ protofibril antibody is BAN2401. In some embodiments, the therapeutically effective amount of at least one anti-Aβ protofibril antibody is 10 mg/kg. In some embodiments, the composition comprising a therapeutically Attorney Docket No.08061.0062-00304 effective amount of at least one anti-Aβ protofibril antibody disclosed herein is administered bi- weekly or monthly. In some embodiments, a composition comprising 10 mg/kg of BAN2401 is administered bi-weekly. In some embodiments, a composition comprising 10 mg/kg of BAN2401 is administered monthly. In some embodiments, an additional biomarker and cerebrospinal fluid level of phospho- Tau, may be used to select a patient for treatment, to allow for monitoring and treatment decisions such as whether to increase or decrease the amount of antibody being administered, determine whether to increase or decrease the frequency of administration, determine whether to introduce a further therapeutic agent, determine whether to switch to a maintenance dose, and/or whether to discontinue treatment with the anti-Aβ protofibril antibody. In some embodiments, an improvement in an additional biomarker, in combination with a decreasing cerebrospinal fluid level of phospho-Tau over the same period, may indicate an effective treatment. In some embodiments, an improvement in an additional biomarker, in combination with a decreasing cerebrospinal fluid level of phospho-Tau over the same period, may indicate an effective treatment. In some embodiments, an improvement in an additional biomarker, in combination with a decreased cerebrospinal fluid level of phospho-Tau relative to an untreated control, may indicate an effective treatment. In some embodiments, an indication of the efficacy of treatment may be used to decrease the amount of antibody being administered, decrease the frequency of administration, or to switch to a maintenance dose. h. Brain Volume In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in an improvement, relative to placebo, of total hippocampal atrophy as measured by volumetric MRI (vMRI). In some embodiments, a subject’s brain volume (e.g., total ventricular volume, left and/or right ventricular volume, total volume, right and/or left hippocampal volumes, cortical thickness) is measured before treatment. In some embodiments, a subject’s brain volume (e.g., total ventricular volume, left and/or right ventricular volume, total volume, right and/or left hippocampal volumes, cortical thickness) is measured at 6,12, and/or 18 months after treatment. In some embodiments, administration to a subject of a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody disclosed herein results in an improvement, relative to placebo, of brain volume atrophy as measured by vMRI. 10. Subjects having AD, suspected of having AD, or at risk of developing AD Subjects treated herein include those having AD or suspected of having AD. In some embodiments, the subject shows changes (e.g., an increase, a decrease, a change in the rate and/or extent of an increase, or a change in the rate and/or extent of the decrease) in one or more biomarkers associated with AD pathology (e.g., the biomarkers described above), as compared with a reference Attorney Docket No.08061.0062-00304 measurement. In some embodiments, the reference measurement may be a measurement taken from the same subject, e.g., at an earlier point in time, or a measurement in a part of the subject’s body, tissue, or fluids where the biomarkers levels do not change in response to AD pathology. In some embodiments, the reference measurement may be a measurement taken from another subject, such as a healthy control subject, or may be an average of measurements taken from more than one reference subject. In some embodiments, the subject may show a change and/or a difference in a measurement of one or more biomarkers associated with AD pathology prior to treatment, e.g., one or more of (a) increased amyloid in the brain, e.g., as measured by amyloid PET (e.g., a centiloid measure of about 20-40, e.g., a centiloid measure of about 20-32), (b) increased tau in the brain, e.g., as measured by positron emission tomography (PET), (c) decreased cerebrospinal fluid levels of Aβ1- 42 (e.g., a decreased ratio of Aβ1-42/1-40) and/or increased total tau, phosphorylated tau isoforms (e.g., p-tau181, p-tau217, and/or p-tau231, the ratio of p-tau181/np-tau181, and/or the ratio of p- tau217/np-tau217), neurogranin, and/or neurofilament light chain (NfL), and (d) decreased blood serum or plasma levels of Aβ1-42 (e.g., a decreased ratio of Aβ1-42/1-40 in the plasma or serum), and/or increased total tau, phosphorylated tau (P-tau) isoforms (e.g., P-tau181, P-tau217, and/or P- tau231), ratio of P-tau181/NP-tau181, and/or ratio of P-tau217/NP-tau217, glial fibrillary acidic protein (GFAP), and/or neurofilament light chain (NfL), as compared to a reference measurement (e.g., measurement from a healthy control). In some embodiments, the subject may show a change in the ratio of phosphorylated to non-phosphorylated Tau 217 (P-Tau217/NP-Tau217 ratio, also called P-Tau217R or pTau217R) in blood plasma or serum, e.g., the ratio may be increased in subjects who have, are suspected of having, or are at risk of developing AD. Without being bound by theory, biomarkers as disclosed herein may be effective for predicting amyloid PET status (Rissman et al., 2024, Alzheimers & Dementia, 20(2): 1214-1224; Janelidze et al., 2022, Alzhimer’s & Dementia, 18:283-293) and for detecting and diagnosing AD (Hampel et al., 2023, Neuron, 111(18):2781-2799). In some embodiments, at least one of p-tau217/np-tau217, Aβ42/Aβ40, and p-tau181/np-tau181 may be used to predict amyloid PET status. In some embodiments, a measurement of p-tau217 and/or Aβ42/Aβ40 may be used to predict amyloid PET status. In some embodiments, a combination of p- tau217 and Aβ42/Aβ40 may be used to predict amyloid PET status. In some embodiments, the ratios of p-tau217/np-tau217 and Aβ42/Aβ40 may be used in combination to predict amyloid PET status. In some embodiments, the subject is amyloid-positive, e.g., as indicated by a PET assessment, a CSF assessment of Aβ(1-42), MRI, and/or retinal amyloid accumulation. In some embodiments, a subject has AD, e.g., has been diagnosed with AD. For example, the subject may have been diagnosed with (a) mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood and/or has been diagnosed as having mild Alzheimer’s disease dementia; (b) Attorney Docket No.08061.0062-00304 mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by National Institute of Aging – Alzheimer’s Association (NIA-AA) core clinical criteria; (c) mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by a CDR global score of 0.5 and a Memory Box score of 0.5 or greater before treatment; (d) mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by a history of subjective memory decline with gradual onset and slow progression over the last 1 year before treatment, e.g., as corroborated by an informant; (e) mild Alzheimer’s disease dementia by the NIA-AA core clinical criteria for probable Alzheimer’s disease dementia; or (f) mild Alzheimer’s disease dementia by a CDR score of 0.5 to 1.0 and a Memory Box score of 0.5 or greater before treatment. In some embodiments, the subject has early AD. The subject with early AD may have symptoms ranging in severity from mild cognitive impairment due to AD – intermediate likelihood to mild Alzheimer’s disease dementia. In some embodiments, subjects with early AD have MMSE scores of 22 to 30 and Clinical Dementia Rating (CDR) global range 0.5 to 1.0. In some embodiments, a subject is suspected of having AD, e.g., based on one or more biomarkers and/or cognitive symptoms of dementia. In some embodiments, a subject is at risk for developing AD but has not yet exhibited cognitive symptoms of dementia. For example, a subject may have risk factors related to age or genetic mutations. In some embodiments, the subject is ApoE4-positive. In some embodiments, the subject is at least 65 years old, e.g., 65 to 80 years old. In some embodiments, the subject is 55 to 64 years old and has at least one risk factor chosen from: (i) a first degree relative diagnosed with dementia onset before age 75; (ii) at least one apolipoprotein E4 variant (APOE4) allele; and (iii) elevated brain amyloid according to PET or cerebrospinal fluid (CSF) testing. In some embodiments, a subject at risk for AD has elevated brain amyloid, e.g., as measured by and/or confirmed by PET assessment, but does not exhibit any detectable cognitive symptoms. In some embodiments, a subject at risk for AD has a change in a biomarker such as amyloid PET; tau in the brain, e.g., as measured by positron emission tomography (PET), cerebrospinal fluid levels of one or more of Aβ1-42 (or a ratio of Aβ1-42/1-40 in the cerebrospinal fluid), total tau, phosphorylated tau (P-tau) isoforms (e.g., P- tau181, P-tau217, and/or P-tau231), the ratio of P-tau181/NP-tau181, the ratio of P-tau217/NP- tau217, neurogranin, and neurofilament light chain (NfL), and/or a change in a blood serum or plasma levels of one or more of Aβ1-42 (or a ratio of Aβ1-42/1-40), total tau, phosphorylated tau (P-tau) isoforms (e.g., P-tau181, P-tau217, and/or P-tau231), the ratio of P-tau181/NP-tau181, and/or the ratio of P-tau217/NP-tau217, glial fibrillary acidic protein (GFAP), and/or neurofilament light chain (NfL), relative to a control subject or population. In some embodiments, a subject at risk for developing AD may have pre-AD (also referred to as preclinical AD, in which subjects are cognitively unimpaired but have elevated amyloid in the Attorney Docket No.08061.0062-00304 brain, e.g., as based on a change in one or more biomarkers associated with AD pathology). For example, the subject may show a change in one or more biomarkers associated with AD pathology, but no cognitive impairment, e.g., as measured by clinical symptoms of AD. In some embodiments, the subject has a Global Clinical Dementia Rating (CDR) score of 0. In some embodiments, the subject has a Mini-Mental State Examination (MMSE) score greater than or equal to 27, with educational adjustments. In some embodiments, the subject has a Wechsler Memory Scale-IV Logical Memory (subscale) II (WMS-IV LMII) score better than one standard deviation below age-adjusted mean in the WMS-IV LMII; namely a score of greater than 15 for a subject of age ranging from 50 to 64 years, of greater than 12 for a subject of age ranging from 65 to 69 years, of greater than 11 for a subject of age ranging from 70 to 74 years, of greater than 9 for a subject of age ranging from 75 to 79 years, and of greater than 7 for a subject of age ranging from 80 to 90 years. 11. Anti-Aβ protofibril antibodies In some embodiments, an antibody binding to Aβ (also called an anti-Aβ antibody) is an antibody that binds to any form (e.g., conformation) of Aβ, such as Aβ monomers, oligomers (e.g., different forms of Aβ oligomers such as dimers, trimers, tetramers, pentamers, hexamers, nonamers, dodecamers), a paranucleus (e.g., a partially-folded monomer that forms a nucleus for fibril elongation), protofibrils, or mature fibrils. In some embodiments, an anti-Aβ antibody may bind to more than one form of Aβ. For example, an exemplary anti-Aβ antibody may be a pan-Aβ antibody, such as a pan-AβpE3 antibody that reacts with high molecular weight oligomers, protofibrils, and fibrillar forms of Aβ that are found in different plaque types. In some embodiments, an anti-Aβ antibody may bind preferentially to a specific form of Aβ. For example, an exemplary Aβ antibody may be an anti-Aβ protofibril antibody that binds to at least to protofibrils. In some embodiments, an anti-Aβ protofibril antibody may bind preferentially to protofibrils and may also bind to other forms of Aβ. In some embodiments, an anti-Aβ protofibril antibody may preferentially bind to protofibrils as compared to other forms of Aβ. In some embodiments, an anti-Aβ protofibril antibody may preferentially bind to protofibrils, and not to other forms of Aβ. In some embodiments, any anti-Aβ protofibril antibody may be used in the methods disclosed herein. In some embodiments, the antibody comprises one or more of the sequences listed in Tables 1-4, e.g., comprising a complete set of 6 complementarity determining regions (CDRs) and/or a complete set of variable regions and/or a complete set of heavy and light chain sequences from the tables. In some embodiments, the anti-Aβ protofibril antibody comprises three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 1 (HCDR1), SEQ ID NO: 2 (HCDR2), and SEQ ID NO: 3 (HCDR3); and three light chain complementarity determining regions (LCDR1 , LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 4 (LCDR1), SEQ ID NO: 5 (LCDR2), and SEQ ID NO: 6 Attorney Docket No.08061.0062-00304 (LCDR3). In some embodiments, the anti-Aβ protofibril antibody comprises a heavy chain variable region comprising an amino acid sequence of SEQ ID NO: 7 and a light chain variable region comprising an amino acid sequence of SEQ ID NO: 8. In some embodiments, the anti-Aβ protofibril antibody comprises human heavy and light chain variable region frameworks. In some embodiments, the anti-Aβ protofibril antibody comprises a human IgG1 heavy chain constant region, and a human Ig kappa light chain constant region. In some embodiments, the anti-Aβ protofibril antibody comprises a heavy chain comprising an amino acid sequence of SEQ ID NO: 9 and a light chain comprising an amino acid sequence of SEQ ID NO: 10. “CDRs” used herein in the context of an antibody sequence or structure refers to complementarity determining regions, that provide the main determinants of antigen binding. Generally, the antigen-binding site has six CDRs; three in the VH (HCDR1, HCDR2, HCDR3), and three in the VL (LCDR1, LCDR2, LCDR3). The CDRs may be determined according to the Kabat numbering scheme. which may be determined by according to the Kabat numbering scheme (Kabat et al., Sequences of Proteins of Immunological Interest, 5th Ed. Public Health Service, National Institutes of Health, Bethesda, Md., 1991, hereafter referred to as “Kabat report”). In some embodiments, the at least one anti-Aβ protofibril antibody comprises a human constant region. In some embodiments, the human constant region of the at least one anti-Aβ protofibril antibody comprises a heavy chain constant region chosen from IgG1, IgG2, IgG3, IgG4, IgM, IgA, IgE, and any allelic variation thereof as disclosed in the Kabat report. Any one or more of such sequences may be used in the present disclosure. In some embodiments, the heavy chain constant region is chosen from IgG1 and allelic variations thereof. The amino acid sequence of human IgG1 constant region is known in the art and set out in SEQ ID NO: 11. In some embodiments, the human constant region of the at least one anti-Aβ antibody comprises a light chain constant region chosen from κ-λ-chain constant regions and any allelic variation thereof as discussed in the Kabat report. Any one or more of such sequences may be used in the present disclosure. In some embodiments, the light chain constant region is chosen from κ and allelic variations thereof. The amino acid sequence of human κ chain constant region is known in the art and set out in SEQ ID NO: 12. In some embodiments, the at least one anti-Aβ protofibril antibody is BAN2401, also known as lecanemab. The terms “BAN2401” and “lecanemab” are used interchangeably and refer to a humanized IgG1 monoclonal version of mAb158, which is a murine monoclonal antibody raised to target protofibrils and disclosed in WO 2007/108756 and Journal of Alzheimer’s Disease 43: 575-588 (2015). BAN2401 comprises three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 1 (HCDR1), SEQ ID NO: 2 (HCDR2), and SEQ ID NO: 3 (HCDR3); and three light chain complementarity determining regions Attorney Docket No.08061.0062-00304 (LCDR1 , LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 4 (LCDR1), SEQ ID NO: 5 (LCDR2), and SEQ ID NO: 6 (LCDR3) and is described in WO 2007/108756 and in Journal of Alzheimer’s Disease 43:575-588 (2015). BAN2401 comprises (i) a heavy chain variable region comprising the amino acid sequence of SEQ ID NO: 7 and (ii) a light chain variable region comprising the amino acid sequence of SEQ ID NO: 8. The full length sequences of heavy chain and light chain of BAN2401 are set forth in SEQ ID NOs: 9 and 10 and are described in WO 2007/108756 and in Journal of Alzheimer’s Disease 43:575-588 (2015). In some embodiments, the isolated anti-Aβ protofibril antibody to be used in treatment is present in a concentration of at least 80 mg/mL. In some embodiments, the isolated anti-Aβ protofibril antibody is present in a concentration of at least 100 mg/mL. In some embodiments, the isolated anti- Aβ protofibril antibody is present in a concentration of at least 200 mg/mL. In some embodiments, the isolated anti-Aβ protofibril antibody is present in a concentration of at least 250 mg/mL. In some embodiments, the isolated antibody or fragment thereof is present in a concentration ranging from 80 mg/mL to 300 mg/mL. In some embodiments, the isolated anti-Aβ protofibril antibody is present in a concentration ranging from 85 mg/mL to 275 mg/mL. In some embodiments, the isolated anti-Aβ protofibril antibody is present in a concentration ranging from 90 mg/mL to 250 mg/mL. In some embodiments, the isolated anti-Aβ protofibril antibody is present in a concentration ranging from 95 mg/mL to 225 mg/mL. In some embodiments, the isolated anti-Aβ protofibril antibody is present in a concentration ranging from 100 mg/mL to 200 mg/mL. In some embodiments, the isolated antibody or fragment thereof is present in a concentration of 80 mg/mL, 90 mg/mL, 100 mg/mL, 110 mg/mL, 120 mg/mL, 130 mg/mL, 140 mg/mL, 150 mg/mL, 160 mg/mL, 170 mg/mL, 180 mg/mL, 190 mg/mL, 200 mg/mL, 210 mg/mL, 220 mg/mL, 230 mg/mL, 240 mg/mL, 250 mg/mL, 260 mg/mL, 270 mg/mL, 280 mg/mL, 290 mg/mL, or 300 mg/mL. In some embodiments, the isolated antibody or fragment thereof is present in a concentration of 100 mg/mL. In some embodiments, the isolated antibody or fragment thereof is present in a concentration of 200 mg/mL. In some embodiments, the isolated antibody or fragment thereof is present in a concentration of 250 mg/mL. In some embodiments, the isolated antibody or fragment thereof is present in a concentration of 300 mg/mL. In some embodiments, the isolated antibody or fragment thereof is BAN2401. As used herein, a “fragment” of an antibody comprises a portion of the antibody, for example comprising an antigen- binding or a variable region thereof. Non-limiting examples of fragments include Fab fragments, Fab' fragments, F(ab')2 fragments, Fv fragments, diabodies, linear antibodies, and single-chain antibody molecules. 12. Therapeutically effective amount of at least one anti-Aβ protofibril antibody In various embodiments, the methods of the present disclosure comprise administering to a subject a composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril Attorney Docket No.08061.0062-00304 antibody. As used herein, the term a “therapeutically effective amount” refers to an amount of a compound or pharmaceutical composition sufficient to produce a desired therapeutic effect. One of ordinary skill in the art will understand that the therapeutically effective amount of the at least one anti-Aβ protofibril antibody administered to a subject may depend upon a number of factors including pharmacodynamic characteristics, route of administration, frequency of treatment, and health, age, and weight of the subject to be treated and, with the information disclosed herein, will be able to determine the appropriate amount for each subject. In some embodiments, the therapeutically effective amount is a dose chosen to improve efficacy and/or maintain efficacy and improve at least one of safety and tolerability. In some embodiments, the therapeutically effective amount is chosen to lower at least one side effect and simultaneously improve efficacy and/or maintain efficacy. Therapeutically effective doses of an anti- Aβ protofibril antibody and methods for measuring treatment efficacy are disclosed in PCT/US2022/073576; PCT/US2022/079571; and PCT/US2022/041926 and are incorporated herein by reference. In some embodiments, 0.5 mg/kg to 45 mg/kg, 0.5 mg/kg to 40 mg/kg, 0.5 mg/kg to 35 mg/kg, 0.5 mg/kg to 30 mg/kg, 0.5 mg/kg to 25 mg/kg, 0.5 mg/kg to 20 mg/kg, 0.5 mg/kg to 15 mg/kg, 0.5 mg/kg to 10 mg/kg, 0.5 mg/kg to 5 mg/kg, or 0.5 mg/kg to 2.5 mg/kg of at least one anti- Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 2.5 mg/kg to 45 mg/kg, 2.5 mg/kg to 40 mg/kg, 2.5 mg/kg to 35 mg/kg, 2.5 mg/kg to 30 mg/kg, 2.5 mg/kg to 25 mg/kg, 2.5 mg/kg to 20 mg/kg, 2.5 mg/kg to 15 mg/kg, 2.5 mg/kg to 10 mg/kg, or 2.5 mg/kg to 5 mg/kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 5 mg/kg to 45 mg/kg, 5 mg/kg to 40 mg/kg, 5 mg/kg to 35 mg/kg, 5 mg/kg to 30 mg/kg, 5 mg/kg to 25 mg/kg, 5 mg/kg to 20 mg/kg, 5 mg/kg to 15 mg/kg, or 5 mg/kg to 10 mg/kg, of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 7.5 mg/kg to 45 mg/kg, 7.5 mg/kg to 40 mg/kg, 7.5 mg/kg to 35 mg/kg, 7.5 mg/kg to 30 mg/kg, 7.5 mg/kg to 25 mg/kg, 7.5 mg/kg to 20 mg/kg, 7.5 mg/kg to 15 mg/kg, or 7.5 mg/kg to 10 mg/kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, from 0.5 mg/kg, 1 mg/kg, 2 mg/kg, 3 mg/kg, 4 mg/kg, 5 mg/kg, 6 mg/kg, 7 mg/kg, 8 mg/kg, 9 mg/kg, 10 mg/kg, 11 mg/kg, 12 mg/kg, 13 mg/kg, 14 mg/kg, 15 mg/kg, 16 mg/kg, 17 mg/kg, 18 mg/kg, 19 mg/kg, 20 mg/kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, up to 20 Attorney Docket No.08061.0062-00304 mg/kg, 19 mg/kg, 18 mg/kg, 17 mg/kg, 16 mg/kg, 15 mg/kg, 14 mg/kg, 13 mg/kg, 12 mg/kg, 11 mg/kg, 10 mg/kg, 9 mg/kg, 8 mg/kg, 7 mg/kg, 6 mg/kg, 5 mg/kg, 4 mg/kg, 3 mg/kg, 2 mg/kg, 1 mg/kg, or 0.5 mg/kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 0.5 mg/kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 1 mg/kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 2 mg/kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 2.5 mg/kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 3 mg/kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 4 mg/kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 5 mg/kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 6 mg/kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 7 mg/kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 7.5 mg/kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 8 mg/kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 9 mg/kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 10 mg/kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 11 mg/kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 12 mg/kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 12.5 mg/kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 13 mg/kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 14 mg/kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 15 mg/kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 16, 17, 18, 19, or 20 mg/kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. In some embodiments, 21, 22, 23, 24, or 25 mg/kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. Attorney Docket No.08061.0062-00304 In some embodiments, 27.5 mg/kg, 30 mg/kg, 32.5 mg/kg, 35 mg/kg, 37.5 mg/kg, 40 mg/kg, 42.5 mg/kg, 45 mg/kg, 47.5 mg/kg, or 50 mg/kg of at least one anti-Aβ protofibril antibody is administered to the subject relative to body weight of the subject. As mentioned, in some embodiments, the at least one anti-Aβ protofibril antibody is BAN2401. Accordingly, in some embodiments, 0.5 mg/kg to 45 mg/kg, 0.5 mg/kg to 40 mg/kg, 0.5 mg/kg to 35 mg/kg, 0.5 mg/kg to 30 mg/kg, 0.5 mg/kg to 25 mg/kg, 0.5 mg/kg to 20 mg/kg, 0.5 mg/kg to 15 mg/kg, 0.5 mg/kg to 10 mg/kg, 0.5 mg/kg to 5 mg/kg, or 0.5 mg/kg to 2.5 mg/kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 2.5 mg/kg to 45 mg/kg, 2.5 mg/kg to 40 mg/kg, 2.5 mg/kg to 35 mg/kg, 2.5 mg/kg to 30 mg/kg, 2.5 mg/kg to 25 mg/kg, 2.5 mg/kg to 20 mg/kg, 2.5 mg/kg to 15 mg/kg, 2.5 mg/kg to 10 mg/kg, or 2.5 mg/kg to 5 mg/kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 5 mg/kg to 45 mg/kg, 5 mg/kg to 40 mg/kg, 5 mg/kg to 35 mg/kg, 5 mg/kg to 30 mg/kg, 5 mg/kg to 25 mg/kg, 5 mg/kg to 20 mg/kg, 5 mg/kg to 15 mg/kg, or 5 mg/kg to 10 mg/kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 7.5 mg/kg to 45 mg/kg, 7.5 mg/kg to 40 mg/kg, 7.5 mg/kg to 35 mg/kg, 7.5 mg/kg to 30 mg/kg, 7.5 mg/kg to 25 mg/kg, 7.5 mg/kg to 20 mg/kg, 7.5 mg/kg to 15 mg/kg, or 7.5 mg/kg to 10 mg/kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, from 0.5 mg/kg, 1 mg/kg, 2 mg/kg, 3 mg/kg, 4 mg/kg, 5 mg/kg, 6 mg/kg, 7 mg/kg, 8 mg/kg, 9 mg/kg, 10 mg/kg, 11 mg/kg, 12 mg/kg, 13 mg/kg, 14 mg/kg, 15 mg/kg, 16 mg/kg, 17 mg/kg, 18 mg/kg, 19 mg/kg, 20 mg/kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, up to 20 mg/kg, 19 mg/kg, 18 mg/kg, 17 mg/kg, 16 mg/kg, 15 mg/kg, 14 mg/kg, 13 mg/kg, 12 mg/kg, 11 mg/kg, 10 mg/kg, 9 mg/kg, 8 mg/kg, 7 mg/kg, 6 mg/kg, 5 mg/kg, 4 mg/kg, 3 mg/kg, 2 mg/kg, 1 mg/kg, or 0.5 mg/kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 0.5 mg/kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 1 mg/kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 2 mg/kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 2.5 mg/kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 3 mg/kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 4 mg/kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 5 mg/kg of BAN2401 is administered to the subject relative to body Attorney Docket No.08061.0062-00304 weight of the subject. In some embodiments, 6 mg/kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 7 mg/kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 7.5 mg/kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 8 mg/kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 9 mg/kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 10 mg/kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 11 mg/kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 12 mg/kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 12.5 mg/kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 13 mg/kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 14 mg/kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 15 mg/kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 16, 17, 18, 19, or 20 mg/kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 21, 22, 23, 24, or 25 mg/kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 27.5 mg/kg, 30 mg/kg, 32.5 mg/kg, 35 mg/kg, 37.5 mg/kg, 40 mg/kg, 42.5 mg/kg, 45 mg/kg, 47.5 mg/kg, or 50 mg/kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 2.5 mg/kg to 10 mg/kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 5 mg/kg to 10 mg/kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 2.5 mg/kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 5 mg/kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 7.5 mg/kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, 10 mg/kg of BAN2401 is administered to the subject relative to body weight of the subject. In some embodiments, a subject is administered a first dose of the anti-Aβ protofibril antibody without an initial titrating step up to the treatment dose (e.g., a subject starts treatment at 10 mg/kg with no titration). In some embodiments, a dose of BAN2401 may be used without the need of a prior titrating step. In some embodiments, a subject is switched to a maintenance dose without an initial titrating step to the maintenance dose. In certain instances, providing a therapeutic dose without a titration step may provide additional therapeutic benefits to the patient, e.g., a faster shift in plasma biomarkers toward amyloid negativity or facilitating identification sooner of patients that do not have a therapeutic change in plasma biomarkers in response to the anti-Aβ protofibril antibody (non- responders) and who would benefit from alternative treatment. Attorney Docket No.08061.0062-00304 13. Dosage Regimens and Routes of Administration In various embodiments, methods are disclosed herein for treating AD that comprise administration of an anti-Aβ protofibril antibody (e.g., BAN2401) to a subject. In some embodiments, the subject has early AD. In some embodiments, a subject who has pre-AD or is suspected of having AD is administered an anti-Aβ protofibril antibody (e.g., BAN2401). In some embodiments, the anti- Aβ protofibril antibody may be administered to a subject according to a dosage regimen (also called a “dosing regimen,” “treatment regimen” or “treatment,”), e.g., a schedule specifying doses of the anti- Aβ protofibril antibody administered per unit of time, including the number of doses over a given time period and the elapsed time between doses. In some embodiments, the dosage regimen comprises administering the anti-Aβ protofibril antibody at a specified dose, according to a schedule (e.g., on a repetitive basis). In some embodiments, the anti-Aβ protofibril antibody may be administered daily, once weekly, also called “weekly”, or every other week, also called “biweekly”, or monthly, also called “every 4 weeks.” In some embodiments, the anti-Aβ protofibril antibody may be administered intravenously and/or subcutaneously. In some embodiments, a dosage regimen comprises administration of at least one initiation dose (also called a treatment dose) and at least one maintenance dose. In some embodiments, the dosing regimen comprises administration of at least one dose of the anti-Aβ protofibril antibody via one route of administration. In some embodiments, the dosing regimen comprises administration of at least one dose of the anti-Aβ protofibril antibody via more than one route of administration (e.g., initially administering an antibody intravenously and then switching to subcutaneous administration). In some embodiments, the anti-Aβ protofibril antibody is administered intravenously, e.g., by an injection into a peripheral vein. In an upper extremity, the median basilic or cephalic veins of the arm or the metacarpal veins in the hand’s dorsum may be used. In a lower extremity, the dorsal venous plexus of the foot may be used. After 18 months, population modeling predicts that reducing the frequency of 10 mg/kg to once every 4 weeks will continue the reduction in amyloid beta plaque levels. In some embodiments, the anti-Aβ protofibril antibody is administered subcutaneously. In a subcutaneous injection, the anti-Aβ protofibril antibody is injected into the tissue layer between the skin and muscle, such as a fatty tissue just below the skin. In some embodiments, the subcutaneous administration is injected into the abdomen (e.g., at or under the level of the belly button), thigh (e.g., front of the thigh), or upper arm (e.g., back or side of the upper arm). In some embodiments, a volume of the injection administered subcutaneously is less than 2 mL. In some embodiments, the anti-Aβ protofibril antibody is subcutaneously administered using a vial and syringe (also called “vial/syringe” or “syringe/vial” or “SC Vial”). For example, the Attorney Docket No.08061.0062-00304 anti-Aβ protofibril antibody in a subcutaneous formulation may be removed from a vial into a syringe and then injected from the syringe into the subject. In some embodiments, the anti-Aβ protofibril antibody is administered using an autoinjector (also called an “auto-injector,” “AI,” “AI Device,” or “SC AI”). An exemplary auto- injector is the YpsoMate™ 2.25 mL AI Device, which has been approved in the United States (US) and Europe as a presentation for Ajovy® (fremanezumabv-frm). In some embodiments, an autoinjector may comprise a plastic PLAJEX™ syringe, a tapered needle (24G-29G), a V spring, a spring force, and component colors. It may be a single-use, disposable injection device consisting of a housing with a content viewing window, a spring activated mechanism, and integrated needle safety feature. In some embodiments, a 2.25 mL PLAJEX™ syringe may be prefilled with the anti-Aβ protofibril antibody. At least one AI Device may be needed to administer the dose of the anti-Aβ protofibril antibody. In some embodiments, the anti-Aβ protofibril antibody is administered intravenously for at least one dose, and subcutaneously for at least one dose. For example, the anti-Aβ protofibril antibody (e.g., BAN2401) may be administered to a subject intravenously, e.g., once weekly, for a period of time, such as 2, 4, 6, 8, 10, 12, 14, 16, 18, 20, 22, or 24 months, after which the antibody may be administered subcutaneously. In some embodiments, the anti-Aβ protofibril antibody may be administered subcutaneously using a vial-syringe, and then later administered subcutaneously using an AI. In some embodiments, the anti-Aβ protofibril antibody may be administered subcutaneously using a vial-syringe or an AI, and then later administered intravenously. In some embodiments, the method of treatment comprises switching between an intravenous or subcutaneous dose, or from an initiation to a maintenance dose, at a set time point (e.g., after 18 months or after 24 months). In some embodiments, the method of treatment comprises using a biomarker level to determine switching between an intravenous or subcutaneous dose or from an initiation to a maintenance dose, e.g., when measured at or after a set time point (e.g., after 18 months or after 24 months). In some embodiments, a maintenance dose is administered subcutaneously (e.g., as one or more subcutaneous injections). In some embodiments, BAN2401 (also called LEQEMBI, lecanemab, or lecanemab-irmb) is supplied as a solution for intravenous use and is a preservative-free, sterile, clear to opalescent and colorless to pale yellow solution for intravenous use by infusion after dilution. In some embodiments, LEQEMBI may be supplied in single-dose vials available in concentration of 500 mg/5 mL (100 mg/mL) or 200 mg/2 mL (100 mg/mL). In some embodiments, each mL of solution contains 100 mg of lecanemab-irmb and arginine hydrochloride (42.13 mg), histidine (0.18 mg), histidine hydrochloride monohydrate (4.99 mg), polysorbate 80 (0.50 mg), and Water for Injection at an approximate pH of 5.0. In some embodiments, LEQEMBI is diluted in 250 mL of 0.9% Sodium Attorney Docket No.08061.0062-00304 Chloride Injection, USP. In some embodiments, a dosage of LEQEMBI is 10 mg/kg, relative to the weight of the subject. a. Initiation Doses In some embodiments, the anti-Aβ protofibril antibody may be administered to a subject (e.g., a subject that has AD, is suspected of having AD, or is at risk for AD) according to a dosage regimen (also called a dosing regimen) in which a dose, e.g., a therapeutically effective dose, is administered at a regular dosing interval on a repetitive basis. In some embodiments, the dose may be called an initiation dose, a treatment dose, or a first dose. The initiation dose may be administered to a subject according to a dosage regimen (e.g., an initiation dosage regimen, also called an initiation dosing regimen) in which initiation dose of the anti-Aβ protofibril antibody may be administered at an interval (e.g., daily, weekly, biweekly, or monthly), for a period of time, e.g., until the subject shows evidence of improved AD pathology and/or slowed progression of AD. In some embodiments, the period of time is at least 18 months or at least 24 months. In some embodiments, the period of time is 18 months. In some embodiments, the period of time is 24 months. In some embodiments, the period of time is about 12 months, 18 months, 24 months, 30 months, 36 months, 42 months, 48 months, 54 months, or 60 months. In some embodiments, the initiation dose may be administered until the subject is amyloid negative. In some embodiments, at least one initiation dose of the anti-Aβ protofibril antibody is administered intravenously to the subject. An exemplary dosage regimen may comprise intravenously administering the anti-Aβ protofibril antibody (e.g., BAN2401) at a dose of 10 mg/kg. In some embodiments, BAN2401 is administered intravenously, once weekly, at a dose of 10 mg/kg, e.g., for at least 18 months or at least 24 months, or e.g., until the subject is amyloid-negative or until one or more other biomarker levels are reached (e.g. a change in a biomarker discussed herein). In some embodiments, BAN2401 is administered intravenously, biweekly, at a dose of 10 mg/kg, e.g., for at least 18 months or at least 24 months, or e.g., until the subject is amyloid-negative, or until one or more other biomarker levels are reached (e.g. a change in a biomarker discussed herein). In some embodiments, at least one initiation dose of the anti-Aβ protofibril antibody (e.g., BAN2401) is administered subcutaneously, e.g., by vial-syringe or by autoinjector. An exemplary dosage regimen may comprise subcutaneously administering the anti-Aβ protofibril antibody (e.g., BAN2401) at a dose of 720 mg. In some embodiments, the dose may be administered in one single injection of 720 mg. In some embodiments, the dose of 720 mg may be administered in two concurrent, e.g., sequential, injections of 360 mg (e.g., 2 x 1.8 mL of 400 mg/2 mL or 2 x 1.8 mL of 200 mg/mL). In some embodiments, BAN2401 is administered subcutaneously, once weekly, at a dose of 720 mg, e.g., for 18 months. In some embodiments, BAN2401 is administered subcutaneously, once weekly, at a dose of 720 mg, e.g., for 24 months. In some embodiments, Attorney Docket No.08061.0062-00304 BAN2401 is administered subcutaneously, once weekly, at a dose of 720 mg, e.g., for at least 18 months or at least 24 months, or e.g., until the subject is amyloid-negative, or until one or more other biomarker levels are reached (e.g., a change in a biomarker discussed herein). In some embodiments, BAN2401 is administered subcutaneously, biweekly, at a dose of 720 mg, e.g., for at least 18 months or at least 24 months, or e.g., until the subject is amyloid-negative, or until one or more other biomarker levels are reached (e.g., a change in a biomarker discussed herein). The dose of 720 mg may be administered in two concurrent, e.g., sequential, injections of 360 mg (e.g., 2 x 1.8 mL of 400 mg/2 mL or 2 x 1.8 mL of 200 mg/mL). In some embodiments, different initiation doses of the anti-Aβ protofibril antibody (e.g., BAN2401) may be administered. In some embodiments, a subcutaneous dose of the anti-Aβ protofibril antibody (e.g., BAN2401) may be administered at more than one dose. For example, a subject may be transitioned from a first dose of the antibody for a first period of time to a second dose of the antibody for a second period of time. For example, a dose of 720 mg may be administered subcutaneously, once weekly, for a first period of time, after which a dose of 500 mg may be administered subcutaneously, once weekly, for a second period of time. In some embodiments, the 720 mg dose is administered in 2 consecutive injections of 360 mg (2x1.8 mg of 200 mg/mL subcutaneous formulation) for the first period of time, and then the 500 mg dose is administered in 2 consecutive injections of 250 mg (2x1.25 mL of 200 mg/mL subcutaneous formulation) for the second period of time. In some embodiments, the first period of time is less than about 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, or 24 months, or less than a period of time until the subject is amyloid negative, or one or more biomarker levels as discussed herein are reached. In some embodiments, the first period of time is less than 18 months. In some embodiments, the second period comprises the first period of time plus the remainder of 18 months, so that the first and second time periods are about 18 months in total. In some embodiments, a subject may receive the subcutaneous dose of 720 mg of the anti-Aβ protofibril antibody (e.g., BAN2401) weekly, via an autoinjector, for a first period of time, and then a subcutaneous dose of 500 mg of the anti-Aβ protofibril antibody (e.g., BAN2401) weekly, via an autoinjector, for a second period of time. In some embodiments, an initiation dosing regimen of the Aβ protofibril antibody (e.g., BAN2401) may comprise administration of the antibody at more than one dose and/or via more than one mode of administration. In some embodiments, a subject may be transitioned from a first dose of the antibody, administered intravenously, for a first period of time, to a second dose of the antibody, administered either intravenously or subcutaneously, for a second period of time. In some embodiments, the subject may be transitioned from a first dose of the antibody, administered intravenously, for a first period of time, to a second dose of the antibody, administered subcutaneously, for a second period of time. For example, a first dose of 10 mg/kg may be administered to the subject intravenously, biweekly, for at first period of time (e.g., 6 months or 12 Attorney Docket No.08061.0062-00304 months), after which a second dose of 720 mg or less (e.g., 500 mg) maybe administered for a second period of time (e.g., 6 months or 12 months). In some embodiments, the initiation dosage regimen comprising a first dose of the Aβ protofibril antibody (e.g., BAN2401) administered intravenously a first period of time, and a second dose of the Aβ protofibril antibody administered subcutaneously for a second period of time may be followed by a maintenance dosing regimen, such as a maintenance dosing regimen comprising subcutaneous administration of the antibody at a dose of 360 mg biweekly, or subcutaneous administration of the antibody at a dose of 250 mg biweekly. In some embodiments, a subject’s exposure to an anti-Aβ protofibril antibody depends on whether the dose was administered using a vial/syringe or an AI. In some embodiments, exposure to the antibody when using an AI is greater than when using a vial/syringe. Accordingly, the dose subcutaneously administered using an AI may be lower than a dose subcutaneously administered using a vial/syringe. In some embodiments, where a target systemic exposure is based on an intravenous administration (e.g., 10 mg/kg biweekly), the exposure from the dose subcutaneously administered using an AI method may be higher than that obtained using a vial/syringe method. Accordingly, the dose administered subcutaneously using an AI may be lower than a dose administered subcutaneously using a vial/syringe. In some embodiments, the systemic exposure from a dose intravenously administered at 10 mg/kg biweekly is about equal to a dose subcutaneously administered at 720 mg weekly using a vial/syringe method, or to a dose subcutaneously administered at 500 mg weekly using an AI method. For example, the dosage of the anti-Aβ protofibril antibody subcutaneously administered using an AI method may be about 40%, 45%, 50%, 60%, 65%, 70%, 75%, 80%, 85%, 90%, or 95% of the dosage subcutaneously administered using a vial/syringe method. In some embodiments, the dosage of the anti-Aβ protofibril antibody subcutaneously administered using an AI method 65%, 66%, 67%, 68%, 69%, or 70% of the dose subcutaneously administered using a vial/syringe method. In some embodiments, at least one initiation dose of the anti-Aβ protofibril antibody (e.g., BAN2401) is administered subcutaneously by autoinjector (AI). An exemplary dosage regimen may comprise subcutaneously administering the anti-Aβ protofibril antibody (e.g., BAN2401) at a dose of 500 mg, e.g., using an AI. The dose of 500 mg may be administered in a single injection of 500 mg. The dose of 500 mg may be administered in two concurrent, e.g., sequential, injections of 250 mg (e.g., 2 x 1.25 mL of 400 mg/2 mL, which is also 2 x 1.25 mL of 200 mg/mL). In some embodiments, BAN2401 is administered subcutaneously using an AI, once weekly, at a dose of 500 mg for 18 months. In some embodiments, BAN2401 is administered subcutaneously using an AI, once weekly, at a dose of 500 mg for 24 months. In some embodiments, BAN2401 is administered subcutaneously using an AI, biweekly, at a dose of 500 mg, e.g., for at least 18 months or at least 24 months, or e.g., until the subject is amyloid-negative. In some embodiments, BAN2401 is administered subcutaneously using an AI, biweekly, at a dose of 500 mg, e.g., for at least 18 months or at least 24 Attorney Docket No.08061.0062-00304 months, or e.g., until the subject is amyloid-negative. The dose of 500 mg may be administered in a single injection of 500 mg. The dose of 500 mg may be administered in two concurrent, e.g., sequential, injections of 250 mg (e.g., 2 x 1.25 mL of 400 mg/2 mL or 2 x 1.25 mL of 200 mg/mL). In some embodiments, at least one of the dose, frequency of administration, or mode of administration of the anti-Aβ protofibril antibody may be selected and/or changed to achieve a target systemic exposure (e.g., AUC) to the antibody. In some embodiments, a target systemic exposure is the same regardless of the mode of administration. For example, an exemplary target systemic exposure may be achieved when the anti-Aβ protofibril antibody is intravenously administered at 10 mg/kg biweekly. The same target systemic exposure may be achieved when the anti-Aβ protofibril antibody is subcutaneously administered at 720 mg, e.g., weekly. In some embodiments, the same target systemic exposure may be achieved when the anti-Aβ protofibril antibody is subcutaneously administered at 500 mg, e.g., weekly. In some embodiments, a patient first receives the anti-Aβ protofibril antibody (e.g., BAN2401) intravenously administered at 10 mg/kg dose, and later receives the antibody subcutaneously administered at a dose (e.g., 720 mg weekly or 500 mg weekly) that achieves about the same target systemic exposure as the intravenous dose. In some embodiments, the anti-Aβ protofibril antibody is subcutaneously administered at a dose (e.g., 720 mg or 500 mg weekly) selected to achieve a target systemic exposure calculated to be equivalent to that achieved by intravenous administration at 10 mg/kg biweekly, whether or not the patient has previously received an intravenous administration of the antibody. In some embodiments, the anti-Aβ protofibril antibody is subcutaneously administered at a dose (e.g., 720 mg or 500 mg) weekly. In some embodiments, the anti-Aβ protofibril antibody is subcutaneously administered at a dose of 500 mg weekly. In some embodiments, the anti-Aβ protofibril antibody is subcutaneously administered at a dose (e.g., 720 mg or 500 mg) biweekly.In some embodiments, administering a low dose of the anti-Aβ protofibril antibody (e.g., in an initiation dose) or reducing the dose (e.g., in either an initiation dose or in a subsequent maintenance dose) may lower or reduce the patient’s risk for developing ARIA, while still retaining the ability to improve AD pathology or slow progression of AD. For example, the dose of the anti-Aβ protofibril antibody may be reduced by lowering the dose in each administration, reducing the frequency of administration, or changing the method of administration. The reduced dose may be adequate to clear Aβ and reduce or slow one or more of tau aggregation, expression of biomarkers of AD, cognitive decline, and/or indicators of AD pathology. In another example, a patient may be on a treatment dose and then moved, e.g., after 18 months or after 24 months of treatment, to a maintenance dose that is lower or administered less frequently while stabilizing or continuing to see reduced levels of brain Aβ protofibril, e.g., as measured by continued changes in amyloid PET scans and/or one or more biomarkers of amyloid.In some embodiments, the subject has AD, is suspected of having AD, or is at risk for AD. In some embodiments, the subject has AD, e.g., early AD. In some embodiments, the subject has pre-AD. Attorney Docket No.08061.0062-00304 b. Maintenance Doses In some embodiments, a maintenance dose of the anti-Aβ protofibril antibody may be administered to the subject (e.g., a subject that has AD, is suspected of having AD, or is at risk for AD). The maintenance dose may be a dose administered to maintain therapeutically effective concentrations of the anti-Aβ protofibril antibody in the subject and/or to maintain or continue to reduce levels of Aβ protofibril in the brain of the treated subject. Without being bound by theory, it has been found by the inventors that after an initiation regimen of an anti-Aβ protofibril antibody such as BAN2401 in a subject, a maintenance dosing regimen may be administered at a reduced frequency or dosage, or a different route of administration, while holding level or continuing to reduce Aβ protofibrils in the brain. In some embodiments, the maintenance dose may be administered to a subject according to a dosage regimen (e.g., a maintenance dosage regimen, also called a maintenance dosing regimen) in which the maintenance dose is administered at a regular interval on a repetitive basis. In some embodiments, each maintenance dose of the anti-Aβ protofibril antibody may be administered daily, weekly, biweekly, or monthly. Administering at least one maintenance dose of the anti-Aβ protofibril antibody, e.g., according to a maintenance regimen which succeeds a treatment regimen, may prevent a return to baseline (e.g., pretreatment) levels of markers of AD pathology. For example, when a treatment regimen is stopped or interrupted, amyloid PET may rebound and/or plasma biomarkers, e.g., the p- tau181 levels and the Aβ42/40 ratio, may return to baseline pre-treatment levels. This effect has been corroborated by predicted rates of early amyloid reaccumulation based on data from gantenerumab and donanemab, as well as observations from a gap period in Study 201, a multicenter, double-blind, placebo-controlled, Phase 2b trial conducted in 856 patients with early AD. A core study in Study 201 evaluated key efficacy assessments, including clinical change on the AD Composite Score (ADCOMS) as the primary endpoint at 12 months and as key secondary endpoints, ADCOMS, Clinical Dementia Rating-Sum-of-Boxes (CDR-SB) and AD Assessment Scale-Cognitive Subscale 14 (ADAS-Cog14) at 18 months. Following analysis of the 18-month core phase, an intervening off- treatment period (gap period) ranging from 9-59 months (mean 24 months) was taken, which was followed by an OLE with 10 mg/kg IV bi-weekly lecanemab dosing to assess long-term safety and tolerability. Subjects who stopped treatment showed an increase in amyloid PET by approximately 7 Centiloids (21% return to pretreatment baseline) and an increase in p-tau181 and the Aβ42/40 ratio indicating return of 24%, and 47%, respectively, to pre-treatment baseline levels. Thus, in some embodiments, continued treatment with at least one maintenance dose of the anti-Aβ protofibril antibody may maintain suppression of the disease progression rate and/or prevent reaccumulation of AD pathology which may occur if treatment is stopped. Attorney Docket No.08061.0062-00304 In some embodiments, a maintenance dose may be administered after a preset time period, e.g., after completion of an initiation dosage regimen. For example, a maintenance dose may be administered after about 18 months of treatment with an initiation dose, or the maintenance dose may be administered after about 24 months of treatment with an initiation dose. In some embodiments, the maintenance dose is administered after about 30 months of treatment with an initiation dose. In some embodiments, the maintenance dose is administered after about 36 months of treatment with an initiation dose. In some embodiments, the maintenance dose is administered after about 48 months of treatment with an initiation dose. In some embodiments, the maintenance dose may be the same as the initiation dose. In some embodiments, a maintenance dose may be lower than the initiation dose. In some embodiments, a maintenance dose may be administered less frequently than the initiation dose. This may reduce the burden for subjects and their caregivers associated with frequent administration of the anti-Aβ protofibril antibody (e.g., BAN2401), while still maintaining the efficacy seen with treatment according to the initiation dose. In some embodiments, the maintenance dose may be administered by a different route of administration than the initiation dose. For example, an initiation dose may be administered intravenously, after which the maintenance dose is administered subcutaneously. In some embodiments, an initiation dose may be administered subcutaneously, after which the maintenance dose is administered intravenously. In some embodiments, the maintenance dose may be administered by the same route of administration as the initiation does. For example, an initiation dose may be administered intravenously, after which the maintenance dose is also administered intravenously. In some embodiments, an initiation dose may be administered subcutaneously, after which a maintenance dose is also administered subcutaneously. In some embodiments, a maintenance dosage regimen comprises administering maintenance doses over a period of time. For example, the maintenance doses may be administered for about 6 months, 12 months, 18 months, 24 months, 30 months, 36 months, 42 months, 48 months, 54 months, 60 months, or for the remainder of the subject’s life. In some embodiments, the maintenance doses are administered until the subject shows evidence of improved AD pathology and/or slowed progression of AD, e.g., until the subject is amyloid negative. In some embodiments, a maintenance dosage regimen comprises administering maintenance doses at intervals. The intervals may be weekly, biweekly, or monthly. In some embodiments, the maintenance dose of the anti-Aβ protofibril antibody (e.g., BAN2401) is 10 mg/kg, administered intravenously. An exemplary maintenance dosage regimen may comprise intravenously administering BAN2401 monthly at dose of 10 mg/kg. In some embodiments, an exemplary maintenance dosage regimen may comprise intravenously administering BAN2401 biweekly at a dose of 10 mg/kg. In some embodiments, an exemplary maintenance dosage regimen Attorney Docket No.08061.0062-00304 may comprise intravenously administering BAN2401 weekly at a dose of 10 mg/kg. In an exemplary embodiment, the initiation dosing regimen comprises intravenously administering BAN2401 biweekly at a dose of 10 mg/kg, and a maintenance dosage comprises intravenously administering BAN2401 every four weeks (monthly) at a dose of 10 mg/kg. In some embodiments, the maintenance dose of the anti-Aβ protofibril antibody (e.g., BAN2401) is 720 mg, administered subcutaneously. In some embodiments, the subcutaneous dose of 720 mg is administered in two concurrent, e.g., sequential injections of 360 mg (e.g., 2 x 1.8 mL of 400 mg/2 mL) of the subcutaneous formulation. An exemplary maintenance dosage regimen may comprise subcutaneously administering BAN2401 weekly at dose of 720 mg. In some embodiments, an exemplary maintenance dosage regimen may comprise subcutaneously administering BAN2401 biweekly at a dose of 720 mg. In some embodiments, the 720 mg dose of BAN2401 is subcutaneously administered, e.g., weekly or biweekly, using a vial-syringe. In some embodiments, the 720 mg dose of BAN2401 is subcutaneously administered, e.g., weekly or biweekly, using an AI. In some embodiments, the maintenance dose of the anti-Aβ protofibril antibody (e.g., BAN2401) is 500 mg, administered subcutaneously. In some embodiments, the subcutaneous dose of 500 mg is administered in two concurrent, e.g., sequential injections of 250 mg (e.g., 2 x 1.25 mL of 400 mg/2 mL) of the subcutaneous formulation. An exemplary maintenance dosage regimen may comprise subcutaneously administering BAN2401 weekly at dose of 500 mg. In some embodiments, an exemplary maintenance dosage regimen may comprise subcutaneously administering BAN2401 biweekly at a dose of 500 mg. In some embodiments, the 500 mg dose of BAN2401 is subcutaneously administered, e.g., weekly or biweekly, using an AI. In some embodiments, the maintenance dose of the anti-Aβ protofibril antibody (e.g., BAN2401) is 360 mg, administered subcutaneously. In some embodiments, the subcutaneous dose is administered in a single injection of 360 mg (e.g., 1 x 1.8 mL of 400 mg/2 mL) of the subcutaneous formulation. An exemplary maintenance dosage regimen may comprise subcutaneously administering BAN2401 weekly at dose of 360 mg. In some embodiments, an exemplary maintenance dosage regimen may comprise subcutaneously administering BAN2401 biweekly at a dose of 360 mg. In some embodiments, the 360 mg dose of BAN2401 is subcutaneously administered, e.g., weekly or biweekly, using an AI. In some embodiments, the 360 mg dose of BAN2401 is subcutaneously administered, e.g., weekly or biweekly, using a vial-syringe. In some embodiments, the maintenance dose of the anti-Aβ protofibril antibody (e.g., BAN2401) is 250 mg, administered subcutaneously. In some embodiments, the subcutaneous dose of 250 mg is administered in a single injection of 250 mg (e.g., 1 x 1.25 mL of 400 mg/2 mL) of the subcutaneous formulation. An exemplary maintenance dosage regimen may comprise subcutaneously administering BAN2401 weekly at dose of 250 mg. In some embodiments, an exemplary maintenance Attorney Docket No.08061.0062-00304 dosage regimen may comprise subcutaneously administering BAN2401 biweekly at a dose of 250 mg. In some embodiments, the 250 mg dose of BAN2401 is subcutaneously administered, e.g., weekly or biweekly, using an AI. In some embodiments, the subject has AD, is suspected of having AD, or is at risk for AD. In some embodiments, the subject has AD, e.g., early AD. In some embodiments, the subject has pre- AD. In some embodiments, the subject receives an initiation dose (e.g., according to an initiation dosing regimen) with a first anti-Aβ protofibril antibody, and then receives a maintenance dose with a second anti-Aβ protofibril antibody. In some embodiments, the first anti-Aβ protofibril antibody may be the same as the second anti-Aβ protofibril antibody, e.g., BAN2401 may be administered during the initiation dose regimen and during the maintenance dose regimen. In some embodiments, the first anti-Aβ protofibril antibody is not the same as the second anti-Aβ protofibril antibody. In some embodiments, the subject receives an initiation dose (e.g., according to an initiation dosing regimen) with a first anti-Aβ antibody and then receives a maintenance dose with a second anti-Aβ antibody, wherein the second Aβ antibody is an anti-Aβ protofibril antibody. In some embodiments, the first anti-Aβ antibody targets at least one form of Aβ, e.g., Aβ monomers, different forms of Aβ oligomers (e.g., dimers, trimers, tetramers, pentamers, hexamers, nonamers, dodecamers), a paranucleus (e.g., a partially-folded monomer that forms a nucleus for fibril elongation), protofibrils, or mature fibrils (Chen et al., 2017, Acta Pharmacologica Sinica, 38, 1205- 1235). In some embodiments, the Aβ monomer may be an Aβ peptides ranging in size from 37-49 residues. In some embodiments, the Aβ monomer is Aβ28, Aβ37, Aβ39, Aβ40 or Aβ42. For example, an exemplary anti-Aβ antibody may bind preferentially to aggregated fibrillar Aβ, to an N-terminally truncated form of Aβ found in amyloid plaque cores, to soluble aggregates of Aβ, to soluble and fibrillar Aβ, and/or to monomeric Aβ. In some embodiments, the anti-Aβ antibody (e.g., aducanumab and gantenerumab) binds preferentially to aggregated fibrillar Aβ, with low affinities for Aβ monomers. For example, aducanumab and gantenerumab may bind preferentially to β-amyloid fibrils over protofibrils. In some embodiments, the anti-Aβ antibody (e.g., donanemab) binds to an N- terminally truncated and pyroglutamated form of Aβ (AβpE3) that is found in amyloid plaque cores. Without being bound by theory, antibodies against AβpE3 may differ in their binding properties to soluble and aggregated conformations of AβpE3-42 (Bouter et al., Acta Neuropathol.2022, 143(5): 601-603). In some embodiments, the anti-Aβ antibody may react with oligomers, protofibrils, and fibrillar forms of Aβ. In some embodiments, the anti-AβpE3 antibody donanemab may react with amyloid plaques in cores. In some embodiments, the anti-Aβ antibody (e.g., bapineuzumab) binds preferentially to soluble and fibrillar Aβ37. In some embodiments, the anti-Aβ antibody (e.g., Attorney Docket No.08061.0062-00304 crenezumab) binds preferentially to multiple forms of aggregated Aβ and to monomers. In some embodiments, the anti-Aβ antibody (e.g., solanezumab) binds preferentially to soluble monomeric Aβ39. In some embodiments, the anti-Aβ antibody is an anti-Aβ protofibril antibody (e.g., lecanemab) that binds preferentially to soluble aggregates of Aβ (protofibrils and oligomers), while also binding moderately to plaques. In some embodiments, the anti-Aβ antibody is associated with a greater risk for ARIA or CAA (Söderberg et al., Scientific Reports, 2024, 14:10868). In some embodiments, a first anti-Aβ antibody (e.g., donanemab) may be administered to clear and/or reduce certain forms of Aβ during the initiation dosage regimen, after which a second anti-Aβ antibody (e.g., an anti-Aβ protofibril antibody, such as BAN2401) may maintain low levels of Aβ during the maintenance dosing regimen, for example, by clearing and/or reducing protofibrils and oligomers and preventing further aggregation into fibrils. In some embodiments, the first anti-Aβ antibody may clear and/or reduce insoluble forms of Aβ, e.g., fibrils and plaques. In some embodiments, the first anti-Aβ antibody is selected from donanemab, aducanumab, bapineuzumab, crenezumab, solanezumab, and gantenerumab. In some embodiments, the first anti-Aβ antibody is donanemab. In some embodiments, the second anti-Aβ antibody is an anti-Aβ protofibril antibody, e.g., it is lecanemab. In some embodiments, the first antibody is donanemab and the second antibody is lecanemab, wherein the lecanemab is administered by iv biweekly or monthly, e.g., at 10 mg/kg. In some embodiments, the first antibody is donanemab and the second antibody is lecanemab, wherein the lecanemab is administered by sc weekly, e.g., at 360 or 250 mg. c. Exemplary Dosage Regimens In some embodiments, a treatment for AD comprises administration of an anti-Aβ protofibril antibody (e.g., BAN2401) according to a dosage regimen comprising at least one initiation dosage regimen. In some embodiments, the dosage regimen comprises only an initiation dosage regimen, e.g., administration of the anti-Aβ protofibril antibody according to a route, frequency, and dose that does not change. In some embodiments, the dosage regimen comprises an initiation dosage regimen and a maintenance dosage regimen. In some embodiments, the initiation dosage regimen and the maintenance dosage regimen differ in at least one of route of administration, frequency of administration, and dose administered at each interval. In some embodiments, a dosage regimen comprises intravenously administering BAN2401 biweekly to a subject (e.g., a subject that has AD, is suspected of having AD, or is at risk for AD) at a dose of 10 mg/kg, e.g., for at least 18 months, 24 months, or e.g., until the subject is amyloid- negative, before switching to less frequent (e.g., monthly) intravenously administered maintenance dose, e.g., a dose of 10 mg/kg. Attorney Docket No.08061.0062-00304 In some embodiments, a dosage regimen comprises intravenously administering BAN2401 biweekly to a subject (e.g., a subject that has AD, is suspected of having AD, or is at risk for AD) at a dose of 10 mg/kg, e.g., for at least 18 months, 24 months, or e.g., until the subject is amyloid- negative, before switching to an intravenously administered maintenance dose of 10 mg/kg, administered once monthly. In some embodiments, a dosage regimen comprises intravenously administering BAN2401 biweekly to a subject (e.g., a subject that has AD, is suspected of having AD, or is at risk for AD) at a dose of 10 mg/kg, e.g., for at least 6 months, 18 months, or at least 24 months or e.g., until the subject is amyloid-negative, before switching to a weekly, subcutaneously administered maintenance dose, e.g., a dose of 360 mg. The weekly maintenance dose of 360 mg may be administered using an AI. In some embodiments, a dosage regimen comprises intravenously administering BAN2401 biweekly to a subject (e.g., a subject that has AD, is suspected of having AD, or is at risk for AD) at a dose of 10 mg/kg, e.g., for at least 6 months, 18 months, or at least 24 months or e.g., until the subject is amyloid-negative, before switching to a weekly, subcutaneously administered maintenance dose, e.g., a dose of 250 mg. The weekly maintenance dose of 250 mg may be administered using an AI. In some embodiments, the dosage regimen comprises subcutaneously administering BAN2401 weekly to a subject (e.g., a subject that has AD, is suspected of having AD, or is at risk for AD), using either a vial-syringe or an AI, e.g., at a dose of 720 mg, e.g., for at least 18 months or at least 24 months or e.g., until a patient is amyloid-negative, before switching to a weekly subcutaneous maintenance dose, e.g., a dose of 360 mg, administered using an AI. In some embodiments, the dosage regimen comprises subcutaneously administering BAN2401 weekly to a subject (e.g., a subject that has AD, is suspected of having AD, or is at risk for AD), using either a vial-syringe or an AI, e.g., at dose of 720 mg administered in two concurrent, e.g., sequential, injections of 360 mg (2 x 1.8 mL of 400 mg/2 mL) of the subcutaneous formulation, e.g., for at least 18 months or at least 24 months, before switching to a weekly, subcutaneously administered maintenance dose, e.g., a dose of 360 mg, administered using an AI, e.g., in one injection of 1.8 mL of 400 mg/2 mL. In some embodiments, the dosage regimen comprises subcutaneously administering BAN2401 weekly to a subject (e.g., a subject that has AD, is suspected of having AD, or is at risk for AD), using an AI, e.g., at a dose of 500 mg, e.g., for at least 18 months or at least 24 months or e.g., until a patient is amyloid-negative, before switching to a weekly subcutaneous maintenance dose, e.g., a dose of 360 mg, administered using an AI. In some embodiments, the dosage regimen comprises subcutaneously administering BAN2401 weekly to a subject (e.g., a subject that has AD, is suspected of having AD, or is at risk for Attorney Docket No.08061.0062-00304 AD), using an AI, e.g., at dose of 500 mg administered in two concurrent, e.g., sequential, injections of 250 mg (2 x 1.25 mL of 400 mg/2 mL) of the subcutaneous formulation, e.g., for at least 18 months or at least 24 months, before switching to a weekly, subcutaneously administered maintenance dose, e.g., a dose of 360 mg, administered using an AI. In some embodiments, the dosage regimen comprises subcutaneously administering BAN2401 weekly to a subject (e.g., a subject that has AD, is suspected of having AD, or is at risk for AD), using an AI, e.g., at a dose of 500 mg, e.g., for at least 18 months or at least 24 months or e.g., until a patient is amyloid-negative, before switching to a weekly subcutaneous maintenance dose, e.g., a dose of 250 mg, administered using an AI. In some embodiments, the dosage regimen comprises subcutaneously administering BAN2401 weekly to a subject (e.g., a subject that has AD, is suspected of having AD, or is at risk for AD), using an AI, e.g., at dose of 500 mg administered in two concurrent, e.g., sequential, injections of 250 mg (2 x 1.25 mL of 400 mg/2 mL) of the subcutaneous formulation, e.g., for at least 18 months or at least 24 months, before switching to a weekly, subcutaneously administered maintenance dose, e.g., a dose of 250 mg, administered using an AI, e.g., in one injection of 1.25 mL of 400 mg/2 mL. Alternatively, in any of the embodiments discussed above, the maintenance dose may be administered to the subject biweekly instead of weekly. In some embodiments, a dosage regimen comprises subcutaneously administering (e.g., via a vial or an autoinjector method) an anti-Aβ protofibril antibody (e.g., administering BAN2401) to a subject (e.g., a subject that has AD, is suspected of having AD, or is at risk for AD) at a dose 400- 800 mg, e.g., 720 mg or 500 mg, e.g., at 500 mg, e.g., for at least 18 months or at least 24 months or until the subject is amyloid negative, before switching to a subcutaneous maintenance dosage regimen. In some embodiments, dosage regimen comprises subcutaneously administering BAN2401 weekly to a subject (e.g., a subject that has AD, is suspected of having AD, or is at risk for AD), e.g., by weekly subcutaneous injection of 500 mg before switching to a weekly subcutaneous maintenance dosage regimen. In some embodiments, a dosage regimen comprises subcutaneously administering BAN2401 weekly to a subject (e.g., a subject that has AD, is suspected of having AD, or is at risk for AD), e.g., by weekly subcutaneous injection of 500 mg in two concurrent, e.g., sequential, injections of 250 mg (e.g., 2 x 1.25 mL of 400 mg/2 mL) before switching to a subcutaneous maintenance dosage regimen. In some embodiments, the subcutaneous maintenance dose is 180 mg. In some embodiments, the subcutaneous maintenance dose is 250 mg. In some embodiments, the subcutaneous maintenance dose is 360 mg. In some embodiments, the subcutaneous maintenance dose is 500 mg. In some embodiments, the maintenance dose is administered weekly. In some embodiments, a subcutaneous maintenance dose of 250 mg is administered weekly. Attorney Docket No.08061.0062-00304 In some embodiments, a dosage regimen comprises subcutaneously administering BAN2401 biweekly to a subject (e.g., a subject that has AD, is suspected of having AD, or is at risk for AD), e.g., at a dose 400-800 mg, e.g., 720 mg or 500 mg, e.g., at a dose of 500 mg, e.g., for at least 18 months or at least 24 months or until a patient is amyloid-negative, before switching to a subcutaneous maintenance dosage regimen, e.g., comprising a maintenance dose of 250 mg, 360 mg, or 500 mg administered biweekly. In some embodiments, a dosage regimen comprises subcutaneously administering BAN2401 biweekly to a subject (e.g., a subject that has AD, is suspected of having AD, or is at risk for AD) using a vial-syringe, e.g., at a dose of 500 mg, e.g., for at least 18 months or at least 24 months or until the subject is amyloid-negative, before switching to a weekly subcutaneous maintenance dosage regimen, e.g., comprising a maintenance dose of 250 mg, 360 mg, or 500 mg administered biweekly using a vial-syringe. In some embodiments, a dosage regimen comprises subcutaneously administering BAN2401 biweekly to a subject (e.g., a subject that has AD, is suspected of having AD, or is at risk for AD) using an AI, e.g., at a dose of 500 mg, e.g., for at least 18 months or at least 24 months or until the subject is amyloid-negative, before switching to a biweekly subcutaneous maintenance dosage regimen, e.g., comprising a maintenance dose of 250 mg, 360 mg, or 500 mg administered biweekly using an AI. In some embodiments, any dose (e.g., 500 mg, 360 mg, or 250 mg) may be administered in a single injection. In some embodiments, a dosage regimen comprises subcutaneously administering BAN2401 biweekly to a subject (e.g., a subject that has AD, is suspected of having AD, or is at risk for AD) using an vial-syringe, e.g., a biweekly subcutaneous injection of 500 mg in two concurrent, e.g., sequential, injections of 250 mg (2 x 1.25 mL of 400 mg/2 mL), e.g., for at least 18 months or at least 24 months, before switching to a biweekly maintenance dosage regimen, e.g., comprising a maintenance dose of 250 mg, 360 mg, or 500 mg administered weekly using a vial-syringe. In some embodiments, any dose (e.g., 500 mg, 360 mg, or 250 mg) may be administered in a single injection. In some embodiments, a dosage regimen comprises subcutaneously administering BAN2401 biweekly to a subject (e.g., a subject that has AD, is suspected of having AD, or is at risk for AD) using an AI, e.g., weekly subcutaneous injection of 500 mg in two concurrent, e.g., sequential, injections of 250 mg (e.g., 2 x 1.25 mL of 400 mg/2 mL), e.g., for at least 18 months, or at least 24 months, or until the subject is amyloid-negative, before switching to a biweekly subcutaneous maintenance dosage regimen, e.g., comprising a maintenance dose of 250 mg, 360 mg, or 500 mg administered weekly using an AI. In some embodiments, a maintenance dose may be administered to a subject weekly, biweekly, or monthly. In some embodiments, dosage regimens may be interchanged. In some embodiments, intravenously administered doses and subcutaneously administered doses may be interchanged at any time. For example, a subject may initially receive one or more initiation dose of the antibody administered intravenously (e.g., 10 mg/kg biweekly), and then transition to further initiation doses of the antibody administered subcutaneously (e.g., 720 mg, 500 mg, 360 mg, or 250 mg) using a Attorney Docket No.08061.0062-00304 vial/syringe or an AI. In some embodiments, a subject may initially receive one or more initiation doses of the antibody subcutaneously (e.g., 720 mg, 500 mg, 360 mg, or 250 mg) using a vial/syringe or an AI, and then transition to further initiation doses of the antibody administered intravenously (e.g., 10 mg/kg biweekly). In some embodiments, one or more initiation doses may be administered intravenously, while one or more maintenance doses may be administered subcutaneously. In some embodiments, one or more initiation doses may be administered subcutaneously, while one or more maintenance doses may be administered intravenously. In some embodiments, a treatment for AD may be administered to a subject (e.g., a subject that has AD, is suspected of having AD, or is at risk for AD) according to an exemplary regimen in the table below. Table 10. Exemplary initiation and maintenance dosage regimens R^{egimen Initiation Dosage Regimen Maintenance Dosage Regimen} M_{ode Quantity Frequency Duration Mode Quantity Frequency Duration} I 1 k Bi kl 1 24 I 1 k M hl A

Attorney Docket No.08061.0062-00304 R^{egimen Initiation Dosage Regimen Maintenance Dosage Regimen} M_{ode Quantity Frequency Duration Mode Quantity Frequency Duration} b SC 500 mg Weekly 18 – 24 SC 360 mg Weekly Any

, g g , , y Alzheimer’s disease, comprises administering BAN2401 at a first dose (e.g., an initiation dose) for a first period of time and then at a second dose (e.g., a maintenance dose) for a second period of time. In some embodiments, a maintenance dose of the anti-protofibril Aβ antibody (e.g., BAN2401) may be the same as an initiation dose but administered less frequently. For example, the initiation dose may be administered weekly, while the maintenance dose is administered biweekly or monthly. In some embodiments, a maintenance dose of the anti-protofibril Aβ antibody (e.g., BAN2401) may be a lower dose than the initiation dose. For example, the initiation dose may be administered at a dose of 500 mg, while a maintenance dose is administered at a dose of 250 mg, or 360 mg. In some embodiments, a maintenance dose of the anti-protofibril Aβ antibody (e.g., BAN2401) may be administered using a different method than an initiation dose. For example, the maintenance dose may be administered by an autoinjector, while the initiation dose was administered by intravenous infusion or subcutaneous vial and syringe injection. In some embodiments, a maintenance dose of the anti-protofibril Aβ antibody (e.g., BAN2401) of 250 mg, 360 mg, or 500 mg may be subcutaneously administered by autoinjector after an initiation dose was intravenously administered (e.g., at a dose of 10 mg/kg biweekly). In some embodiments, a maintenance dose of the anti-protofibril Aβ antibody (e.g., BAN2401) of 250 mg, 260 mg, or 500 mg may be subcutaneously administered by autoinjector after an initiation dose was subcutaneously administered by vial and syringe (e.g., at an initiation dose of 720 mg or 500 mg). In some embodiments, the method of treatment comprises using a biomarker level, e.g., a change in a biomarker indicating that the subject may be switched to a maintenance intravenous or subcutaneous dose. In some embodiments, the biomarker is measured at or after a set time point (e.g., after 18 months or after 24 months). In some embodiments, the change in the biomarker is measured relative to a reference measurement, such as a baseline measurement from the subject prior to treatment. In some embodiments, the change in the biomarker is at least one of decreased amyloid in the brain, e.g., as measured by amyloid PET (e.g., a centiloid measure of about 20-40, e.g., a centiloid Attorney Docket No.08061.0062-00304 measure of about 20-32); decreased tau in the brain, e.g., as measured by positron emission tomography (PET), decreased cerebrospinal fluid levels of one or more of Aβ1-42 (e.g., or a ratio of Aβ1-42/1-40 in the cerebrospinal fluid), total tau, phosphorylated tau (P-tau) isoforms (e.g., P-tau181, P-tau217, and/or P-tau231), the ratio of P-tau181/NP-tau181, the ratio of P-tau217/NP-tau217, neurogranin, and neurofilament light chain (NfL), and/or a change in a blood serum or plasma levels, e.g., an increase in Aβ1-42 (e.g., an increase in a ratio of Aβ1-42/1-40), a decrease in total tau, phosphorylated tau (P-tau) isoforms (e.g., P-tau181, P-tau217, and/or P-tau231), the ratio of P- tau181/NP-tau181, the ratio of P-tau217/NP-tau217, glial fibrillary acidic protein (GFAP), and/or neurofilament light chain (NfL). In some embodiments, treating a subject having Alzheimer’s disease, Pre-AD, or early Alzheimer’s disease comprises intravenously administering BAN2401 and then using a change in a measurement of a biomarker to determine switching from an initiation dosage regimen to a maintenance dosage regimen (e.g., reducing the frequency of administration, changing the route or administration, and/or reducing the dose administered). 14. Composition comprising at least one anti-Aβ protofibril antibody In some embodiments, the at least one anti-Aβ protofibril antibody is comprised in a composition. In some embodiments, the composition consists of at least one anti-Aβ protofibril antibody. In some embodiments, the antibody is present at a concentration of 50-250 mg/ML, e.g., 100-200 mg/mL. In some embodiments, the composition comprises at least one anti-Aβ protofibril antibody and further comprises at least one additional active and/or inactive component. In some embodiments, the at least one additional component can comprise one or more suitable physiologically acceptable excipients for human and/or veterinary use. The compositions of the present disclosure may be in the form of a tablet, pill, capsule, solution, and/or any other suitable form deemed appropriate by one of ordinary skill in the art. The route of administration of the compositions of the present disclosure may be any suitable route, including intravenous, subcutaneous, oral, and nasal. In some embodiments, the composition is formulated as a sterile, non-pyrogenic liquid for intravenous administration. In some embodiments, the composition is a saline solution. In some embodiments, the at least one additional component in the composition comprises buffer(s). In some embodiments, the at least one additional component comprises emulsifier(s). In some embodiments, the at least one additional component comprises sodium citrate, sodium chloride, histidine, arginine, arginine hydrochloride, and/or polysorbate 80. In some embodiments, the sodium citrate may be present at a concentration ranging from 1 mM to 150 mM. In some embodiments, the sodium citrate may be present at a concentration of 25 mM. In some embodiments, the sodium citrate may be present at a concentration of 50 mM. In some embodiments, the sodium chloride may be Attorney Docket No.08061.0062-00304 present at a concentration ranging from 25 mM to 250 mM. In some embodiments, the arginine may be present at a concentration ranging from 240 mM to 360 mM. In some embodiments, the arginine hydrochloride may be present at a concentration ranging from 100 mM to 250 mM. In some embodiments, the histidine may be present at a concentration ranging from 10 mM to 50 mM. In some embodiments, the sodium citrate may be present at a concentration of 125 mM. In some embodiments, the polysorbate 80 may be present at a concentration ranging from 0.001% (w/v) to 2% (w/v). In some embodiments, the polysorbate 80 may be present at a concentration of 0.02% (w/v). In some embodiments, the polysorbate 80 may be present at a concentration of 0.05% (w/v). In some embodiments, the composition is a liquid dosage form comprising at least one anti-Aβ protofibril antibody, such as BAN2401, and further comprising, for instance, sodium citrate, sodium chloride, and polysorbate 80. In some embodiments, the composition is a liquid dosage form comprising 50 mmol/L citrate, 350 mmol/L arginine, and 0.05% polysorbate 80. In some embodiments, the composition is a liquid dosage form comprising at least one anti-Aβ protofibril antibody, such as BAN2401, and further comprising, for instance, arginine hydrochloride, histidine, and polysorbate 80. In some embodiments, the composition is a liquid dosage form comprising 25 mmol/L histidine, 200 mmol/L arginine, 0.05% polysorbate 80. PCT/IB2021/000155 (WO2021/186245) is incorporated herein by reference for suitable intravenous and subcutaneous formulations. 15. Concomitant administration of at least one anti-Aβ protofibril antibody and at least one Alzheimer’s disease medication other than BAN2401 In some embodiments, provided herein is a method of treating a subject, e.g., one having Pre-AD or early Alzheimer’s disease, comprising administering a therapeutically effective amount of at least one anti-Aβ protofibril antibody such as BAN2401 and a therapeutically effective amount of at least one Alzheimer’s disease medication other than BAN2401. In some embodiments, provided herein is a method of reducing and/or slowing clinical decline in a subject, e.g., one having Pre-AD or early Alzheimer’s disease, comprising administering a therapeutically effective amount of at least one anti-Aβ protofibril antibody such as BAN2401 and a therapeutically effective amount of at least one Alzheimer’s disease medication other than BAN2401. The at least one additional therapy may comprise an additional anti-Aβ antibody such as aducanumab. In some embodiments, the at least one additional therapy may comprise a BACE inhibitor and/or an anti-tau antibody. In some embodiments, the at least one Alzheimer’s disease medication is chosen from elenbecestat, donepezil, galantamine, memantine, and rivastigmine. In some embodiments, the at least one Alzheimer’s disease medication is a combination of donepezil and memantine. In some embodiments, the at least one additional therapeutic agent comprises one or more of BACE inhibitors, gamma secretase inhibitors, gamma secretase modulators, Aβ peptide generation inhibitors other than Attorney Docket No.08061.0062-00304 said at least one anti-Aβ protofibril antibody, agents that lower Aβ peptide levels other than said at least one anti-Aβ protofibril antibody, and a combination thereof. In some embodiments, the at least one additional therapeutic agent is a BACE inhibitor. In some embodiments, the BACE inhibitor is chosen from CNP520, BI-1181181, LY2886721, LY3202626, PF-06751979, RG7129, atabecestat, elenbecestat, lanabecestat, and verubecestat. In some embodiments, the BACE inhibitor is elenbecestat. In some embodiments, the BACE inhibitor is chosen from CNP520, BI-1181181, LY2886721, LY3202626, PF-06751979, RG7129, atabecestat, elenbecestat, lanabecestat, and verubecestat. In some embodiments, provided herein is a method of treating a subject having pre-AD, or a patient that is symptomatic for Alzheimer’s disease (e.g., early Alzheimer’s disease), comprising administering a therapeutically effective amount of at least one anti-Aβ protofibril antibody such as BAN2401 and a therapeutically effective amount of an anti-tau antibody or antigen binding fragment thereof that is capable of binding to human tau, e.g., the anti-tau antibody or antigen binding fragment comprises E2814 or an antigen binding fragment thereof. In some embodiments, the anti-tau antibody is an antibody that binds to the microtubule binding region of tau (MTBR-tau). In some embodiments, the anti-tau antibody is E2814. In some embodiments, the anti-tau antibody is LY3303560, ABBV- 8E12, BIIB076, PNT001, UCB0107 PRX005, Lu AF87908, BIIB092, RO7105705, or JNJ-63733657. E2814 is disclosed in US 2019/0112364 A1 as clone 7G6-HCzu25/LCzu18, the sequences of which are incorporated by reference herein. In some embodiments, provided herein is a method of reducing and/or slowing clinical decline in a subject, e.g., one having pre-AD, or a patient that is symptomatic for Alzheimer’s disease (e.g., early Alzheimer’s disease), comprising administering a therapeutically effective amount of at least one anti-Aβ protofibril antibody such as BAN2401 and a therapeutically effective amount of an anti-tau antibody or antigen binding fragment thereof that is capable of binding to human tau, e.g., the anti-tau antibody or antigen binding fragment comprises E2814 or an antigen binding fragment thereof. E2814 is disclosed in US 2019/0112364 A1 as clone 7G6-HCzu25/LCzu18, the sequences of which are incorporated by reference herein. In some embodiments, the isolated anti- tau antibody or antigen binding fragment thereof that is capable of binding to human tau comprises six CDRs (HCDR1, HCDR2, HCDR3, LCDR1, LCDR2, and LCDR3) comprising the amino acid sequences of SEQ ID NO:15 (HCDR1), SEQ ID NO:16 (HCDR2), SEQ ID NO:17 (HCDR3), SEQ ID NO:18 (LCDR1), SEQ ID NO:19 (LCDR2), and SEQ ID NO:20 (LCDR3). See, e.g., Table 6. In some embodiments, the isolated anti-tau antibody or antigen binding fragment thereof that is capable of binding to human tau comprises six CDRs (HCDR1, HCDR2, HCDR3, LCDR1, LCDR2, and LCDR3) from a heavy chain variable region of SEQ ID NO: 21 and a light chain variable region of SEQ ID NO: 22. In some embodiments, the anti-tau antibody or antigen binding fragment thereof that is capable of binding to human tau comprises a heavy chain variable region of SEQ ID NO: 21 and a light chain variable region of SEQ ID NO: 22. See, e.g., Table 7. In some embodiments, the heavy Attorney Docket No.08061.0062-00304 chain constant region comprises SEQ ID NO: 23. In some embodiments, the heavy chain constant region comprises SEQ ID NO: 24. See, e.g., Table 8. In some embodiments, a patient that is symptomatic for Alzheimer’s disease is administered the anti-Aβ protofibril antibody (e.g., BAN2401) for at least 24 weeks then administered the isolated anti-tau antibody or antigen binding fragment thereof that is capable of binding to human tau (e.g., E2814) in conjunction with the isolated anti-Aβ protofibril antibody. In some embodiments, a patient that is symptomatic for Alzheimer’s disease is administered the anti-Aβ protofibril antibody, e.g., for 24 weeks or until the patient’s biomarker status is improved relative to a control subject having AD who does not receive the treatment. The patient is then administered the isolated anti-tau antibody or antigen binding fragment thereof that is capable of binding to human tau in conjunction with the isolated anti-Aβ protofibril antibody. In some embodiments, a patient that is symptomatic for Alzheimer’s disease is administered the anti-Aβ protofibril antibody for 24 weeks or until the patient is amyloid negative, then administered the isolated anti-tau antibody or antigen binding fragment thereof that is capable of binding to human tau in conjunction with the isolated anti-Aβ protofibril antibody. In some embodiments, the patient is asymptomatic for Alzheimer’s disease (pre-AD) and is first administered an isolated anti-tau antibody or antigen binding fragment thereof that is capable of binding to human tau (e.g., E2814), e.g., for 52 weeks before being administered the isolated anti- tau antibody or antigen binding fragment thereof that is capable of binding to human tau in conjunction with an isolated anti-Aβ protofibril antibody (e.g., BAN2401). In some embodiments, such a subject is identified based on a tau PET level higher than in a control subject who does not have pre-AD. In some embodiments, a patient that is asymptomatic for Alzheimer’s disease is administered the isolated anti-tau antibody or antigen binding fragment thereof that is capable of binding to human tau for 52 weeks or until the patient’s rate of increase in tau PET is reduced relative to a control subject having AD who does not receive the treatment, then administered the isolated anti-tau antibody or antigen binding fragment thereof that is capable of binding to human tau in conjunction with the isolated anti-Aβ protofibril antibody. In some embodiments, a patient that is asymptomatic for Alzheimer’s disease is administered the isolated anti-tau antibody or antigen binding fragment thereof that is capable of binding to human tau for 52 weeks or until the patient is amyloid negative, then administered the isolated anti-tau antibody or antigen binding fragment thereof that is capable of binding to human tau in conjunction with the isolated anti-Aβ protofibril antibody. As used herein, the term “Amyloid PET” refers to Amyloid positron emission tomography imaging. In some embodiments, PET imaging (also referred to as a PET scan) is performed to assess for amyloid pathology. In some embodiments, amyloid PET is assessed with a PET tracer and uses Attorney Docket No.08061.0062-00304 the same tracer in follow-up assessments. In some embodiments, the PET imaging uses a florbetapir tracer. In some embodiments, the PET imaging uses a flutemetamol tracer. Amyloid positron emission tomography (PET) imaging can be used to confirm the presence of amyloid pathology in the brain of early AD subjects in the screening phase of the study and/or to evaluate the effects of the at least one anti-AB antibody on amyloid levels in the brain, both by whole brain analysis (e.g., the average of 5-6 cortical regions) and brain region analysis. In some embodiments, the PET scan uses florbetapir. In some embodiments, amyloid plaque load can be identified by a PET imaging uptake visual read, e.g., by a trained radiologist. In some embodiments, 2 readers (1 designated as Primary Reader) visually assess the images to determine whether the scan is positive or negative for amyloid. In further embodiments, four regions of the brain are assessed for uptake of the imaging agent: the temporal lobes, the occipital lobes, the prefrontal cortex, and the parietal cortex and a positive amyloid scan has either 1 region with intense gray matter uptake that is greater than the white matter uptake and extends to the outer edges of the brain, or 2 regions with areas of reduced gray-white contrast. In further embodiments, if disagreement occurs between 2 readers, both meet to review the scan for a consensus read. In some embodiments, amyloid plaque load can be identified by a standard uptake value ratio (SUVr) as compared to a reference region. Methods for calculating amyloid PET SUVr are known in the art and may include those described herein. In some embodiments, a Standard Uptake Value Ratio Quantitative analysis of amyloid levels is completed using PMOD Biomedical Image Quantification Software (PMOD Technologies, Zurich, Switzerland). In some embodiments, PET images are first assessed for subject movement in the X, Y, and Z planes and corrected for motion, if needed, before individual images (e.g., 5-minute emission frames) are averaged, e.g., using a PMOD Averaging Function (PET frames averaged to increase the signal to noise ratio). In some embodiments, corresponding MRIs from subjects are prepared (e.g., using matrix size reduction processing, cropping of the MRI to include only the brain, segmentation to separate images into binary maps of gray matter, white matter, and CSF, and stripping the image of skull leaving only brain mask). In some embodiments, the averaged PET images and prepared MRIs are matched using the PMOD Matching Function, placing the images in the same orientation. In some embodiments, a Brain Normalization function, e.g., as provided by PMOD software, is used along with Brain Norm and Rigid Matching transformation matrices, to produce an averaged PET. In some embodiments, this averaged PET which is normalized to the MNInst space (Senjem et al, 2005) that is in the same orientation as the subject’s segmented MRI for quantitative analysis. In some embodiments, the PMOD Mask Function is used to mask the brain and zero the image outside of the mask to create a Normalized Gray Matter PET and a Normalized White Matter PET. Standard uptake values (SUVs) may be calculated for all gray matter mapped regions and the 3 white matter regions (pons, cerebellar white, and subcortical white) using PMOD software calculated using the normalized PET, subject Attorney Docket No.08061.0062-00304 weight, and injected dose of tracer to arrive at the units of SUVs. In some embodiments, the SUVr is the ratio of the global cortical average as compared to a reference region of choice. In some embodiments, a whole cerebellum mask is used as the reference region. In some embodiments, the reference region is subcortical white matter, derived whole cerebellum, whole cerebellum adjusted by subcortical white matter, cerebellar gray matter, and composite reference regions consisting of cerebellar cortex, pons subcortical white matter, and cerebella white matter. In some embodiments, after administration of the first dose of the composition the adjusted mean change from baseline in a subject’s amyloid PET SUVr value is reduced by at least - 0.10, at least -0.15, at least -0.20, at least -0.25, at least -0.30, at least -0.35, at least -0.40, at least - 0.45, at least -0.50, at least -0.55, at least -0.60, at least -0.65, at least -0.70, at least -0.75, at least - 0.80, at least -0.85, at least -0.90, or at least -0.95 relative to baseline. In some embodiments, the adjusted mean change from baseline in a subject’s amyloid PET SUVr value is reduced by -0.20 to - 0.30. In some embodiments, the amyloid beta plaque levels in the brain are evaluated using PET imaging. In some embodiments, the PET imaging uses a florbetapir tracer. In some embodiments, the PET imaging used a flutemetamol tracer. In some further embodiments, different tracers may yield different results. In some embodiments, the adjusted mean reduction threshold is dependent upon the tracer used. In some embodiments, comparing global cortical average versus whole cerebellum reference, the adjusted mean change from baseline in a subject’s amyloid PET SUVr value is reduced by at least -0.20, such as at least -0.25, after 12 months of administration of the composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody. In some embodiments, the adjusted mean change from baseline in a subject’s amyloid PET SUVr value is reduced by at least -0.25, such as at least -0.30, after 18 months of administration of the composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody. In some embodiments, the reduction of amyloid in the brain is determined by imaging using binding of radiotracers for brain Aβ amyloid and visualized with PET. In some embodiments, the reduction in the adjusted mean change from baseline is at least -50, such as at least -55 or at least - 59 centiloid after 12 months of administration of the composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody. In some embodiments, the reduction in the adjusted mean change from baseline is at least -60, such as at least -65 or at least -70 centiloid after 18 months of administration of the composition comprising a therapeutically effective amount of at least one anti-Aβ protofibril antibody. In some embodiments, said method results in an increased cerebrospinal fluid Aβ1-42 level relative to the cerebrospinal fluid Aβ1-42 level prior to said administration. In some embodiments, said method results in an increase of cerebrospinal fluid Aβ1-42 level of at least 1%, at Attorney Docket No.08061.0062-00304 least 2%, at least 3%, at least 4%, at least 5%, at least 6%, at least 7%, at least 8%, at least 9%, at least 10%, at least 11%, at least 12%, at least 13%, at least 14%, at least 15%, at least 16%, at least 17%, at least 18%, at least 19%, at least 20%, at least 21%, at least 22%, at least 23%, at least 24%, at least 25%, at least 26%, at least 27%, at least 28%, at least 29%, at least 30%, at least 31%, at least 32%, at least 33%, at least 34%, at least 35%, at least 36%, at least 37%, at least 38%, at least 39%, at least 40%, at least 41%, at least 42%, at least 43%, at least 44%, at least 45%, at least 46%, at least 47%, at least 48%, at least 49%, at least 50%, at least 51%, at least 52%, at least 53%, at least 54%, at least 55%, at least 56%, at least 57%, at least 58%, at least 59%, at least 60%, at least 61%, at least 62%, at least 63%, at least 64%, at least 65%, at least 66%, at least 67%, at least 68%, at least 69%, at least 70%, at least 71%, at least 72%, at least 73%, at least 74%, at least 75%, at least 76%, at least 77%, at least 78%, at least 79%, at least 80%, at least 81%, at least 82%, at least 83%, at least 84%, at least 85%, at least 86%, at least 87%, at least 88%, at least 89%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100% relative to the cerebrospinal fluid Aβ1-42 level prior to said administration. In some embodiments, administration of the composition results in a brain amyloid level reduction of -0.20 to -0.45, such as from -0.25 to -0.35 as determined by visual reads of amyloid PET images, wherein the subject is ApoE4-positive. In some embodiments, administration of the composition results in a brain amyloid level reduction of at least -0.25, as determined by visual reads of amyloid PET images, wherein the subject is ApoE4-positive. In some embodiments, administration of the composition results in a brain amyloid level reduction of at least 0.30, as determined by visual reads of amyloid PET images, wherein the subject is ApoE4-positive. In some embodiments, a subject’s brain amyloid level is determined by visual reads of amyloid PET images and expressed as a PET standard uptake value ratio (SUVr value). In some embodiments, administration of the composition results in a brain amyloid level reduction, as measured by an amyloid PET SUVr value, of at least -0.01, at least -0.02, at least -0.03, at least -0.04, at least -0.05, at least -0.06, at least -0.07, at least -0.08, at least -0.09, at least -0.10, at least -0.11, at least -0.12, at least -0.13, at least -0.14, at least -0.15, at least -0.16, at least -0.17, at least -0.18, at least -0.19, at least -0.20, at least -0.21, at least -0.22, at least -0.23, at least -0.24, at least -0.25, at least -0.26, at least -0.27, at least -0.28, or at least -0.29 relative to placebo, wherein the subject is ApoE4-negative. In some embodiments, administration of the composition results in a brain amyloid level reduction of -0.10 to -0.40, as measured by an amyloid PET SUVr value, wherein the subject is ApoE4-negative. In some embodiments, administration of the composition results in a brain amyloid level reduction of at least -0.20, as measured by an amyloid PET SUVr value, wherein the subject is ApoE4-negative. In some embodiments, administration of the composition results in a brain amyloid Attorney Docket No.08061.0062-00304 level reduction of at least -0.25, as measured by an amyloid PET SUVr value, wherein the subject is ApoE4-negative. In some embodiments, a subject’s brain amyloid level is determined by visual reads of amyloid PET images and expressed as a PET standard uptake value ratio (SUVr value). In some embodiments, administration of the composition results in a brain amyloid level reduction of -0.10 to -0.40, as measured by an amyloid PET SUVr value, wherein the subject is ApoE4-negative. In some further embodiments, the subject has an increase in the Aβ42/40 ratio after administration of the first dose of the composition comprising the anti-Aβ protofibril antibody, e.g., an increase to a ratio of about 0.05-0.1, e.g., about 0.08-0.1, e.g., about 0.092, indicating a change from amyloid positive to amyloid negative in the brain of the subject. In some further embodiments, the subject has an increase in the Aβ42/40 ratio after administration of the first dose of the composition comprising the anti-Aβ protofibril antibody, e.g., an increase to a ratio above 0.092, indicating a change from amyloid positive to amyloid negative in the brain of the subject. In some embodiments, the subject has an increase in the Aβ42/40 ratio after 6 months or after 12 months or after 18 months or after 24 months of administration of the first dose of the composition comprising the anti-Aβ protofibril antibody, e.g., an increase to a ratio of about 0.05-0.1, e.g., about 0.08-0.1, e.g., about 0.092, indicating a change from amyloid positive to amyloid negative in the brain of the subject. In some embodiments, the subject has an increase in the Aβ42/40 ratio after 6 months or after 12 months or after 18 months or after 24 months of administration of the first dose of the composition comprising the anti-Aβ protofibril antibody, e.g., an increase to a ratio above 0.092, indicating a change from amyloid positive to amyloid negative in the brain of the subject. In some embodiments, an increase in the Aβ42/40 ratio indicates a reduction in brain amyloid level, as determined by visual reads of amyloid PET images. In some embodiments, a subject with a reduction in brain amyloid level is given a reduced dose or frequency of the anti-Aβ protofibril antibody, alone or in combination with at least one additional therapy, e.g., a BACE inhibitor and/or anti-tau antibody.

Attorney Docket No.08061.0062-00304 SEQUENCE TABLES Table 1. Amino acid sequences of monoclonal antibody (mAb)CDRs mAb IgG chain SEQ ID NO Amino acid sequence BAN2401 HCDR1 1 SFGMH

abe . mno acd sequences o m b varabe regons mAb IgG chain SEQ ID NO Amino acid sequence S E H S Y

Attorney Docket No.08061.0062-00304 Table 3. Amino acid sequences of mAb heavy and light chains mAb IgG chain SEQ ID NO Amino acid sequence BAN2401 Heavy chain 9 EVQLVESGGGLVQPGGSLRLSCSASGFTF

Attorney Docket No.08061.0062-00304 Table 4. Amino acid sequences of mAb constant regions mAb IgG chain Class SEQ ID NO Amino acid sequence BAN2401 Heavy chain IgG1 11 ASTKGPSVFPLAPSSKSTSGGTAA T E P V R P V K R S L H

Attorney Docket No.08061.0062-00304 Table 5. Amino acid sequences of Amyloid β Amyloid β SEQ ID NO Amino acid sequence Amyloid β 1-42 13 DAEFRHDSGYEVHHQKLVFFAEDVGSNK K

. q mAb IgG chain SEQ ID NO Amino acid sequence

Table 7. Amino acid sequences of E2814 variable regions mAb IgG chain SEQ ID NO Amino acid sequence T Y D S S

Attorney Docket No.08061.0062-00304 Table 8. Amino acid sequences of E2814 constant regions mAb IgG chain Class SEQ ID NO Amino acid sequence E2814 Heavy chain IgG1 23 ASTKGPSVFPLAPSSKSTSGGTAA T E P V R P V K R S L H

Attorney Docket No.08061.0062-00304 Table 9. Amino acid sequence of Tau SEQ ID NO Amino acid sequence Tau 25 MAEPRQEFEVMEDHAGTYGLGDRKDQGGYTMHQDQEGDTDAG Q D P Q D N S

Attorney Docket No.08061.0062-00304 EXAMPLES The present disclosure is further illustrated by the following examples that should not be construed as limiting. The contents of all references, patents, and published patent applications cited throughout this application, as well as the figures, are incorporated herein by reference in their entirety for all purposes. Example 1: Study 301 The safety and efficacy of lecanemab was evaluated in a double-blind, placebo-controlled, parallel-group, randomized study (Study 301 CLARITY AD, NCT 03887455) in patients with Alzheimer’s disease (patients with confirmed presence of amyloid pathology and mild cognitive impairment [62%] and mild cognitive impairment [38%], consistent with Stage 3 and Stage 4 Alzheimer’s disease). Patients could enroll in an optional, long-term extension of the study. The primary efficacy outcome was change from baseline at 18 months in the Clinical Dementia Rating scale Sum of Boxes (CDR-SB). Key secondary endpoints included change from baseline at 18 months for the following measures: amyloid Positron Emission Tomography (PET) using centiloids, Alzheimer Disease Assessment Scale – Cognitive Subscale 14 (ADAS-cog14), and Alzheimer's Disease Cooperative Study-Activities of Daily Living Scale for Mild Cognitive Impairment (ADCS MCI-ADL). A total of 1795 patients were enrolled and randomized 1:1 to receive lecanemab 10 mg/kg or placebo once every 2 weeks. Of the total number of patients randomized, 69% were ApoE ε4 carriers and 31% were ApoE ε4 non-carriers. Overall median age of patients was 72 years, with a range to 50 to 90 years. Fifty-two percent were women. Of the global population, 1381 (77%) were White, 303 (17%) Asian, and 47 (2.6%) Black; of the 947 patients in the United States, 895 (94.5%) were White, 213 (22.5%) were Hispanic ethnicity, 43 (4.5%) Black, and 7 (0.7%) Asian. Patients with MCI due to Alzheimer’s disease were enrolled with a CDR global score of 0.5, Memory Box score of 0.5 or greater. Patients with mild AD dementia were enrolled with a global CDR score of 0.5 or 1.0, Memory Box score of 0.5 or greater. All patients had a Mini-Mental State Examination (MMSE) score of ≥22, had objective impairment in episodic memory as indicated by at least 1 standard deviation below age-adjusted mean in the Wechsler-Memory Scale-IV Logical Memory II (subscale) (WMS-IV LMII). The randomization was stratified according to clinical subgroup; the presence or absence of concomitant symptomatic medication for Alzheimer’s disease at baseline (cholinesterase inhibitors and the N-methyl-D-aspartate antagonist memantine); ApoE ε4 carrier status; and region. The mean length of treatment was 16 months (range: 0.5 to 19 months). Attorney Docket No.08061.0062-00304 Lecanemab treatment met the primary endpoint and reduced clinical decline on the global cognitive and functional scale, CDR-SB, compared with placebo at 18 months by 27%, which represents a treatment difference in the score change of -0.45 (p=0.00005). Highly statistically significant differences (p<0.01) between treatment groups were also seen in the results for ADAS-cog14 and ADCS MCI-ADL at 18 months; see Figure 1. Figure 1 shows the results for CDR-SB, ADAS-cog14, and ADCS MCI-ADL in Study 301. Starting as early as six months, across all time points, lecanemab treatment showed statistically significant changes in the primary and all key secondary endpoints from baseline compared to placebo (all p-values <0.01); see Figures 2, 3, 4, 10, and 11. Figure 2 shows the adjusted mean change from Baseline in CDR-SB in Study 301. Figure 3 shows the adjusted mean change from Baseline in CDR-SB in Study 301. Figure 3 shows the adjusted mean change from baseline in CDR-SB in Study 301. Figure 4 shows the adjusted mean change from baseline in ADCS MCI-ADL in Study 301. Figure 11 shows the time to worsening of global CDR scores. Figure 12 shows a slope analysis using CDR-SB (an analysis of the rate of change over time in CDR-SB), based on observed data and an extrapolation to 2 years. The adjusted mean change from baseline, SE and p-value are derived using mixed model for repeated measures with treatment group, visit, treatment group by visit interaction, clinical subgroup, use of Alzheimer’s disease symptomatic medication at baseline, ApoE4 carrier status, region, baseline value by visit interaction as fixed effects, and baseline value as covariate. The change from baseline at 18 months in amyloid (as measured on PET using centiloids) is shown in Figure 5. The reduction in brain amyloid beta plaque is shown as the adjusted mean change from baseline in amyloid beta PET centiloids, as measured in Study 301. As shown in Figure 10, lecanemab slows disease progression, maintaining individuals in earlier stages of disease for longer relative to placebo. Progression was defined as global CDR score progressing from 0.5 [MCI] to 1 [mild AD dementia] or 1 [mild dementia] to 2 [moderate dementia]). Hazard ratio 0.69 (95% CI 0.57-0.83, p=0.00011). Patients on lecanemab had a 31% lower risk of converting to next stage of disease by global CDR. As a result, individuals remain in earlier stages of Alzheimer’s disease for a longer period of time, even within the 18-month course of the study. *Figure 10 uses actual duration for time to event. Including the number at risk within a 2- week window, N at 18 months is 497 in placebo and 527 in LEC10-BW Attorney Docket No.08061.0062-00304 In Figure 11, the rate of change over time (mean slope) based on change from baseline in the CDR-SB was analyzed using linear mixed effects (LME) model. LME model included time, treatment by assessment time as covariate with random intercept and slope. As shown in Figure 11, patients on lecanemab had a 32% slowing of slope annually [(95%CI: 18% to 46%), p=0.00001] vs. placebo. Projected treatment difference at 25.5 months (M) based on slope showed -0.68 treatment difference. Result is increasing separation over time between lecanemab & placebo. Lecanemab takes 25.5 months to reach same level as placebo at 18 months. Change from baseline at 18 months in fluid biomarkers of Alzheimer’s disease pathophysiology showed statistical significance between the lecanemab-treated patients compared to patients on placebo. All biomarker assessments were pre-specified. All fluid biomarkers showed statistically significant improvement except for NfL, which showed a trend at 12 and 18 months (see Table 11). Table 11. Biomarker Results of lecanemab in Study 301 lecanemab 10 mg/kg Biomarker Endpoints biweekly Placebo

Attorney Docket No.08061.0062-00304 lecanemab 10 mg/kg Biomarker Endpoints biweekly Placebo

Attorney Docket No.08061.0062-00304 There was a statistically significant difference in the change from baseline in brain tau pathology in 3 composite regions known to accumulate tau early in the disease (temporal, medial temporal, and meta-temporal) as measured by tau PET SUVR at 18 months in lecanemab 10 mg/kg every two weeks compared to placebo (medial temporal ROI: adjusted mean treatment difference 0.068, p=0.00237; meta temporal ROI: adjusted mean treatment difference 0.071, p=0.01195; temporal ROI: adjusted mean treatment difference 0.065, p=0.01619). The difference was seen as early as 13 months, the first timepoint measured. These changes in Alzheimer’s disease pathophysiologic biomarkers are consistent with biological disease modification with lecanemab treatment. Other prespecified endpoints included the quality of life, caregiver burden, and time to worsening of global CDR scores: European Quality of Life–5 Dimensions 5 Level version [EQ 5D 5L] (patient assessment), Quality of Life in Alzheimer’s Disease (QOL AD)(patient and patient by proxy assessment), and Zarit Burden Interview (study partner burden) (See, Figures 6-9). For all health-related quality of life outcomes there was a statistically significant difference between the lecanemab-treated group compared with the placebo group. Lecanemab reduced the risk of progression to the next stage of AD on the global CDR score by 31% (hazard ratio: 0.69, 95% CI: 0.572, 0.833, p=0.00011) (Figure 1). As shown in Figure 6, at month 18, the adjusted mean change from baseline in EQ-5D-5L by subjects treated with Lecanemab (10 mg/kg biweekly) showed 49% less decline compared to placebo. This effect is consistent across EQ-5D-5L domains. This is consistent across APOE genotypes and range of randomization strata. As shown in Figure 7, at month 18, the adjusted mean change from baseline in QOL-AD by subjects treated with Lecanemab (10 mg/kg biweekly) showed 56% less decline compared to placebo. This effect is consistent across QOL-AD (subject) domains. This is consistent across APOE genotypes and range of randomization strata. As shown in Figure 8, at month 18, the study partner burden as measured by QOL-AD resulted in 23% less decline in subjects treated with Lecanemab (10 mg/kg biweekly). Overall, results reported by subject are generally consistent with results reported by partner. The effect is consistent across domains. This is consistent across APOE genotypes and range of randomization strata. As shown in Figure 9, at month 18, study partner burden as measured by Zarit Burden Interview resulted in 38% less decline in subjects treated with Lecanemab (10 mg/kg biweekly) compared to placebo. Effect consistent across domains. This was consistent across APOE genotypes and range of randomization strata. Attorney Docket No.08061.0062-00304 The results of the Clarity AD QoL measures offer additional evidence for meaningful benefits to patients and care partners of lecanemab treatment beyond benefits demonstrated through cognitive, functional, and biomarker measures. Example 2: Change in Plasma GFAP level with treatment by lecanemab Adjusted mean change from baseline of plasma GFAP level, SE and p-value are derived using mixed model for repeated measures with treatment group, visit, treatment group by visit interaction, clinical subgroup, use of Alzheimer’s disease symptomatic medication at baseline, ApoE4 carrier status, region, baseline value by visit interaction as fixed effects, and baseline value as covariate (Figure 12). In Figure 12, the adjusted mean change from baseline, SE and p-value are derived using mixed model for repeated measures with treatment group, visit, treatment group by visit interaction, clinical subgroup, use of Alzheimer’s disease symptomatic medication at baseline, ApoE4 carrier status, region, baseline value by visit interaction as fixed effects, and baseline value as covariate. Example 3: Incidence of ARIA from Study 301 Monoclonal antibodies directed against aggregated forms of beta amyloid, including lecanemab, can cause amyloid related imaging abnormalities (ARIA), characterized as ARIA with edema (ARIA-E), which can be observed on MRI as brain edema or sulcal effusions, and ARIA with hemosiderin deposition (ARIA-H), which includes microhemorrhage and superficial siderosis. ARIA- H may occur in patients with Alzheimer’s disease. ARIA-H associated with monoclonal antibodies directed against aggregated forms of beta amyloid may occur in association with an occurrence of ARIA-E. ARIA-H of any cause and ARIA-E may occur together. ARIA may be asymptomatic, although serious and life-threatening events, including seizure and status epilepticus, may occur. When present, reported symptoms associated with ARIA may include headache, confusion, visual changes, dizziness, nausea, and gait difficulty. Focal neurologic deficits may also occur. Symptoms associated with ARIA may resolve over time. As described herein, ARIA-Edema (ARIA-E) may be characterized by interstitial vasogenic edema or sulcal effusion that manifests as parenchymal or sulcal hyperintensities. ARIA- Hemorrhages (ARIA-H) may be characterized by micro or macro hemorrhages observed as hypointense hemosiderin deposition in parenchyma or leptomeningeal/subpial space (superficial siderosis). In some embodiments, ARIA is a consequence of the presence of amyloid in cerebral blood vessel walls (cerebral amyloid angiopathy [CAA]). CAA is present pathologically in almost all AD cases, but most patients show no imaging findings (microhemorrhage) or clinical manifestations (intracerebral hemorrhage or inflammatory CAA). There is an increased risk of ARIA with Attorney Docket No.08061.0062-00304 monoclonal antibodies that remove amyloid. There is a lack of definitive clinical criteria for diagnosing CAA, as diagnosis relies on a combination of clinical, pathological, and radiographic measurements. CAA is definitively confirmed by a postmortem examination of the brain. Incidence of ARIA Symptomatic ARIA occurred in 3% (29/898) of patients treated with lecanemab in Study 301. Most of these symptomatic patients (25 of the 29) had ARIA-E with or without concurrent ARIA-H. Clinical symptoms associated with ARIA-E resolved in 96% (24/25) of patients during the period of observation. Including asymptomatic radiographic events, ARIA was observed in 21% (193/898) of patients treated with lecanemab, compared to 10% (85/897) of patients on placebo in Study 301. ARIA-E was observed in 13% (113/898) of patients treated with lecanemab compared with 2% (15/897) of patients on placebo. ARIA-H was observed in 17% (155/898) of patients treated with lecanemab compared with 9% (81/897) of patients on placebo. There was no increase in isolated ARIA-H (i.e., ARIA-H in patients who did not also experience ARIA-E) for lecanemab compared to placebo. Intracerebral hemorrhage greater than 1 cm in diameter was reported in 6 patients in Study 301 after treatment with lecanemab compared to 2 patients on placebo. Events of intracerebral hemorrhage, including fatal events, in patients taking lecanemab have also been reported in other studies. ApoE ε4 Carrier Status and Risk of ARIA In Study 301, 15% (274/1795) of patients in both treatment arms were apolipoprotein E ε4 (ApoE ε4) homozygotes, 53% (957/1795) were heterozygotes, and 31% (564/1795) were noncarriers. The incidence of ARIA was higher in ApoE ε4 homozygotes than in heterozygotes and noncarriers among patients treated with lecanemab. Symptomatic ARIA-E occurred in 9.2% of ApoE homozygotes compared with 1.7% of heterozygotes and 1.4% noncarriers. The recommendations on management of ARIA do not differ between ApoE ε4 carriers and noncarriers. Consider testing for ApoE ε4 status to inform the risk of developing ARIA when deciding to initiate treatment with lecanemab. Radiographic Findings The radiographic severity of ARIA associated with lecanemab was classified by the criteria shown in Table 12. Table 12: ARIA MRI Classification Criteria Attorney Docket No.08061.0062-00304 ARIA Type Radiographic Severity f e

The majority of ARIA-E radiographic events occurred early in treatment (within the first 7 doses), although ARIA may occur at any time and patients may have more than 1 episode. Among the 113 patients with ARIA-E, the maximum radiographic severity of ARIA-E in patients treated with lecanemab was mild in 33% (37/113) of patients, moderate in 58% (66/113) of patients, and severe in 8% (9/113) of patients. Resolution on MRI occurred in 52% of ARIA-E patients by 12 weeks, 81% by 21 weeks, and 100% overall after detection. Among the 80 patients treated with lecanemab who had isolated ARIA-H, 60 of these patients had ARIA-H microhemorrhage. Among these 60 patients, the maximum radiographic severity of ARIA-H microhemorrhage was mild in 87% (52/60), moderate in 12% (7/60), and severe in 2% (1/60) of patients; of the 23 patients with superficial siderosis, 87% (20/23) had mild superficial siderosis. Concomitant Antithrombotic Medication and Other Risk Factors for Intracerebral Hemorrhage In Study 301, baseline use of antithrombotic medication (aspirin, other antiplatelets, or anticoagulants) was allowed if the patient was on a stable dose. The majority of exposures to antithrombotic medications were to aspirin. Antithrombotic medications may not increase the risk of ARIA-E or ARIA-H with lecanemab. Because intracerebral hemorrhages greater than 1 cm in Attorney Docket No.08061.0062-00304 diameter have been observed in patients taking both lecanemab and anticoagulants, additional caution should be exercised when considering the administration of anticoagulants or a thrombolytic agent (e.g., tissue plasminogen activator) to a patient already being treated with lecanemab. Additionally, patients were excluded from enrollment in Study 301 for the following risk factors for intracerebral hemorrhage: prior cerebral hemorrhage greater than 1 cm in greatest diameter, more than 4 microhemorrhages, superficial siderosis, evidence of vasogenic edema, evidence of cerebral contusion, aneurysm, vascular malformation, infective lesions, multiple lacunar infarcts or stroke involving a major vascular territory, and severe small vessel or white matter disease. Caution should be exercised when considering the use of lecanemab in patients with these risk factors. ARIA rates are higher for patients receiving lecanemab compared to those on placebo based on data from the Clarity AD trial. The rates of ARIA (ARIA-E or -H) appear slightly higher in placebo group with concurrent anticoagulants relative placebo subjects not on anticoagulants. ARIA- E, microhemorrhage, and superficial siderosis rates were lower in those treated with lecanemab and either antiplatelet or anticoagulation therapies relative to those treated with lecanemab alone (Figures 13 and 14). Figure 13 shows ARIA rates and antithrombotic use during the CLARITY AD Double- Blind Core period. Figure 14 shows ARIA rates and antithrombotic use during the CLARITY AD Double-Blind Core period by genotype. Results are consistent with overall analysis. The number of intracerebral hemorrhage cases was small, limiting risk assessment of concomitant use. Additional analysis of the Study 301 Core + Open Label Extension (OLE) data is ongoing (Figures 15 and 16) but appear consistent with earlier trial data. Figure 15 shows ARIA rates and antithrombotic use in the CLARITY AD Core and OLE. Figure 16 shows ARIA rates and antithrombotic use during the CLARITY AD Double-Blind Core and OLE by genotype. Results are consistent with overall analysis. In the Clarity AD study, ARIA did not appear more frequently in lecanemab-treated participants on antiplatelet or anticoagulant drugs compared to lecanemab-treated participants that were not on either. ARIA rates are higher in most categories for patients receiving lecanemab compared to those on placebo. There were no differences in the incidence of ARIA-E with antiplatelet drug use. The risks of ARIA (ARIA-E or -H) appear slightly higher in placebo group with concurrent anticoagulants relative to placebo subjects not on anticoagulants. ARIA rates do not appear to be higher with those on lecanemab treated with antiplatelet therapies or with anticoagulation therapies, relative to lecanemab treated subjects not on antithrombotics, but the number of cases was very small. Patients who received lecanemab and an antithrombotic medication (aspirin, other antiplatelets, or Attorney Docket No.08061.0062-00304 anticoagulants) did not have higher ARIA-H rates compared to patients who received placebo and an antithrombotic medication (Figures 13 and 14). Data from a multicenter, double-blind, placebo-controlled, Phase 2b trial conducted in 856 patients with early AD (Study 002) showed that amyloid-related imaging abnormalities-edema (ARIA-E) were dose dependent, with an incidence 9.9% at the highest doses (10 mg/kg lecanemab bi- weekly) for the overall population and 14.3% for ApoE4 positive subjects. Most ARIA-E occurred within 30 days after the initial dose and had mild to moderate severity in radiographic severity. Symptomatic ARIA-E occurred in 3% of participants in the 10 mg/kg lecanemab bi-weekly treatment group. ARIA cerebral microhemorrhages, intracerebral hemorrhage >1cm, and superficial siderosis (ARIA-H) occurred in 6.2% of subjects who received 10 mg/kg biweekly lecanemab and those events were mostly mild in severity. There were no symptomatic cases of ARIA-H reported in the core study. ARIA-E events in the OLE phase were generally consistent with the rate seen in the lecanemab 10 mg/kg biweekly group in the core study. As with the core study, most ARIA-E occurred within 3 months after receiving the initial dose in the OLE and had mostly mild to moderate severity in radiographic severity. ARIA-H events in the OLE were generally consistent with the rate seen in the lecanemab 10 mg/kg biweekly group in the core study. ARIA-H events were mostly mild or moderate in severity. One symptomatic case of ARIA-H, intracerebral hemorrhage > 1cm, was reported in OLE. This subject did not have concurrent ARIA-E, and the adverse event resolved with residual visual field defect. PK/PD modeling showed that the incidence of ARIA-E was correlated with Cmax at steady state. Based on the fact that lecanemab was well tolerated at the highest dose in this study, the Phase 3 Clarity AD study was conducted without dose titration. Subcutaneous formulations that can reduce the Cmax of lecanemab are being developed, suggesting the possibility of reducing the incidence of ARIA-E compared to intravenous formulations. Data from Study 301 is shown in Figure 17 to Figure 30. Figure 17 shows that expected ARIA-E rates for autoinjector are lower than for IV. Exposure-safety models based on combined 201/301 data Subcutaneous (SC) vial exposure based on Study 004 data Autoinjector exposure based on preliminary estimates from Study 005 All simulations assume a population similar to the Study 201/301 patient population Figure 18 shows that all routes of administration are expected to produce similar average steady-state concentrations. Attorney Docket No.08061.0062-00304 The plots in Figure 18 reflect maximum, median, and minimum individual estimates of average steady-state lecanemab concentrations (Css,av). IV data reflects observations from Studies 201/301 in subjects receiving 10 mg/kg Q2W. SC vial and Autoinjector data are extrapolated from Study 005 observations (described below), assuming QW dosing. Figure 19 shows baseline clinical characteristics of Study 301. Figure 20 shows results for primary and key secondary endpoints from Study 301. The results are statistically significant. Figure 21 shows the overall safety profile from Study 301. *There were 2 additional deaths that occurred > 30 days after last study treatment administration (placebo 1, lecanemab 1). Figure 22 shows that in Study 301, incidence of ARIA and infusion-related reactions were different in subjects treated with lecanemab and placebo. Figure 23 shows that in Study 301, 96% of infusion-related reactions were lower grades and usually occurred once early in treatment. Figure 24 shows ARIA-E events in 897 subjects who received a placebo and 898 subjects who received lecanemab. Figure 25A shows that about 90% of ARIA-E cases occurred ≤ 6 months of treatment, and were resolved within 4 months of detection. ARIA-E was screened by MRI at 9 weeks, 13 weeks, 6 months, 12 months, and 18 months. Figure 25B shows long-term ARIA-E probability for subjects who received lecanemab during the Core study. The data indicate that the risk period for ARIA is the first 6 months of treatment, based on vascular amyloid clearance and increased permeability. After 6 months, there were few cases of ARIA-E identified by scheduled MRI, possibly due to vascular remodeling after amyloid clearance. Accordingly, routine MRIs may not be necessary after the 6- month high-risk period. Figure 26 shows that in Study 301, isolated ARIA-H (without ARIA-E) occurred at similar rates between lecanemab and placebo. Figure 27 shows that in Study 301, most ARIA-H events were microhemorrhages and superficial siderosis in conjunction with ARIA-E. Figure 28 shows in Study 301 the rates of ARIA not increased with concurrent antiplatelet or anticoagulant use relative to lecanemab alone. Figure 29 shows event rates of ARIA, ARIA-E, and ARIA-H based on APOE4 carrier status. The event rates of ARIA, ARIA-E, and ARIA-H (including isolated ARIA-H) were generally higher among subjects with baseline microhemorrhage, for each APOE4 group. Attorney Docket No.08061.0062-00304 Figure 30 shows a summary of ARIA cases by number of microhemorrhages at baseline, by APOE4 status. Results from the open label extension (OLE) study were consistent with the results from the Core study 301, as measured by infusion-related reactions, ARIA-E (occurring early in treatment, largely asymptomatic, and resolving spontaneously), ARIA-H (cerebral microhemorrhages and superficial siderosis), and rare intracerebral hemorrhage (ICH) (Honig et al., 2024, Alzheimer’s Research & Therapy, 2024, 16:105 The time to worsening of CDR-SB by 3.0 points was evaluated in subjects who with ARIA and subjects without any ARIA, each of whom received either 10 mg/kg IV administration of lecanemab (LEC10-BW) or placebo. Sensitivity analyses assessing impact on cognition or function showed no impact from ARIA (e.g., multiple imputation techniques (plausible and worst-case scenarios) and ARIA as a covariate (both fixed and time-varying)). There was no accelerated long- term progression for ARIA versus without ARIA conditions, irrespective of threshold. The data indicate that ARIA is not associated with accelerated long-term progression of AD. Figure 50 shows a KM plot of actual duration for time to event. Number at risk includes subjects who did not have the event nor discontinued use of lecanemab by that visit. In summary, lecanemab was generally well-tolerated in elderly population with comorbidities and concomitant medications. Reactions to lecanemab were generally comparable to placebo with exception of ARIA and infusion-related reaction. ARIA and Infusion-Related Reaction generally occurred early in treatment. The data support monitoring of the subjects during the first 6 months of treatment, e.g., according to FDA-approved prescribing information (United States Prescribing Information or USPI) in the US. Abbreviation used in the examples Abbreviation Term A ^ amyloid beta A ^42/40 amyloid beta 42/40 ratio Aβ[1-40] amyloid beta monomer from amino acid 1 to 40 Aβ[1-42] amyloid beta monomer from amino acid 1 to 42 AchEI acetylcholinesterase inhibitor Attorney Docket No.08061.0062-00304 AD Alzheimer’s disease ADA antidrug antibody ADAS-Cog14 Alzheimer Disease Assessment Scale-Cognitive subscale 14-item version ADCOMS Alzheimer’s Disease Composite Score Alzheimer’s Disease Cooperative Study-Activities of Daily Living Scale ADCS MCI-ADL for Mild Cognitive Impairment ADME absorption, distribution, metabolism, and excretion AE adverse event AI autoinjector APC Alzheimer’s prognostic covariate APOE apolipoprotein E APOE4 apolipoprotein E4 ARIA amyloid-related imaging abnormalities ARIA-E amyloid-related imaging abnormality-edema/effusion ARIA-H amyloid-related imaging abnormality-hemorrhage β-hCG beta-human chorionic gonadotropin BAN2401 a humanized IgG1 monoclonal antibody BMI body mass index Cav average concentration CDR Clinical Dementia Rating CDR-SB Clinical Dementia Rating–Sum of Boxes CL clearance COVID-19 Coronavirus Disease 2019 CRA clinical research associate CRF case report form CRO contract research organization CSF cerebrospinal fluid Attorney Docket No.08061.0062-00304 CSR clinical study report C-SSRS Columbia-Suicide Severity Rating Scale DSMB Data Safety Monitoring Board EAD early Alzheimer’s disease eCRF electronic case report form EQ-5D European Quality of Life–5 Dimensions EQ-5D-5L European Quality of Life–5 Dimensions 5 Level version EMA European Medicines Agency FAS full analysis set GDS Geriatric Depression Scale GPSP good postmarketing study practice GVP good vigilance practice hCG human chorionic gonadotropin HCP healthcare professional HRQoL health-related quality of life IA interim analysis iADRS integrated Alzheimer’s Disease Rating Scale ICF informed consent form International Council for Harmonisation of Technical Requirements for ICH Pharmaceuticals for Human Use IEC Independent Ethics Committee IgG immunoglobulin G IgG1 immunoglobulin G1 IP/LC-MS/MS immunoprecipitation liquid chromatography-tandem mass spectrometry INR international normalized ratio IRB Institutional Review Board IUS intrauterine hormone-releasing system Attorney Docket No.08061.0062-00304 IxRS interactive voice and web response system IV intravenous LC-MS/MS liquid chromatography – tandem mass spectrometry LLN lower limit of normal LME linear mixed-effects LNH low, normal, high compared to laboratory reference range LP lumbar puncture LS least squares MAD multiple ascending dose MAR missing at random MCI mild cognitive impairment MedDRA Medical Dictionary for Regulatory Activities MHRA Medicines & Healthcare products Regulatory Agency MI multiple imputations MMRM mixed model for repeated measures MMSE Mini Mental State Examination MPA Medical Products Agency MRI magnetic resonance imaging NAb neutralizing antidrug antibody National Cancer Institute – Common Terminology Criteria for Adverse NCI-CTCAE Events NFL neurofilament light chain NIA-AA National Institute of Aging–Alzheimer’s Association PD pharmacodynamic PET positron emission tomography PG pharmacogenomic PI principal investigator Attorney Docket No.08061.0062-00304 PK pharmacokinetic PMDA Pharmaceuticals and Medical Devices Agency PRN as needed PT preferred term p-tau phosphorylated-tau QOL-AD Quality of Life in Alzheimer’s Disease QTcF corrected QT interval (Fridericia’s Correction Formula) ROI region of interest SAD single ascending dose SAE serious adverse event SAP statistical analysis plan SC subcutaneous system organ class SOP standard operating procedure SMQ Standardised MedDRA Query SUVR standard uptake value ratio TEAE treatment-emergent adverse event TEMAV treatment-emergent markedly abnormal laboratory value TIA transient ischemic attacks t-tau total tau ULN upper limit of normal vMRI volumetric magnetic resonance imaging WMS-IV LMI Wechsler Memory Scale IV-Logical Memory (subscale) I WMS-IV LMII Wechsler Memory Scale IV-Logical Memory (subscale) II Example 4: Phase I Subcutaneous Study (Study 004) Attorney Docket No.08061.0062-00304 BAN2401-A001-004 (Study 004), was a single-center, randomized, open-label, parallel group study that evaluated the absolute bioavailability (BA) of lecanemab following a single fixed dose administered as 700 mg SC injection in the abdomen, compared with a single 10 mg/kg IV dose infused over approximately 1 hour as measured by the ratio of dose normalized AUCinf for subcutaneous versus intravenous dosing. A total of 60 healthy subjects were enrolled in this study with 30 subjects receiving 10 mg/kg IV lecanemab and 29 subjects (as one subject dropped out of study) receiving a fixed 700 mg SC lecanemab via syringe/vial injection. Concentration–time curves following administration of single subcutaneous (700 mg; n = 29) and intravenous doses (10 mg/kg; n=30) in Study 004 are shown in Figure 31. Dose-normalized PK parameters along with 90% CI for AUC are shown in Table 13. Lecanemab half-life was similar following intravenous and subcutaneous administration. After subcutaneous dosing, peak concentrations were achieved approximately 72 hours after injection. The C_max was approximately 4-fold lower for subcutaneous administration compared to intravenous, which reflects the relatively long absorption phase following subcutaneous dose administration compared with 1 hour intravenous infusion. The absolute BA following subcutaneous dose was 49.7% (90% CI:43.5-56.8), indicating a 2-fold lower drug exposure to lecanemab when administered SC compared with intravenous administration. Using this BA value, these results indicate that the weekly subcutaneous dose resulting in equivalent AUC to 10 mg/kg IV for a typical 70 kg subject is approximately 700 mg, which is the actual subcutaneous dose used in Study 004. Of the total 29 subjects included in the SC syringe/vial injection arm, 5 subjects were Japanese, and 24 subjects were non-Japanese. Figure 32 demonstrates that there were no differences in PK between Japanese (n=5) versus non-Japanese (n=24) subjects after a single subcutaneous dose of 700 mg. Table 13 Study 004 Dose-normalized PK Parameters Parameters IV (n=30) SC (n=29) F (%)^a 90% CI

Attorney Docket No.08061.0062-00304 Table 13 Study 004 Dose-normalized PK Parameters Parameters IV (n=30) SC (n=29) F (%)^a 90% CI PK parameters presented as Geometric Mean (CV%) except for t_max as median (min – max).

A: based on analysis of variance (ANOVA); b: n=27. Noting that the lecanemab dose solution is manufactured at a strength of 200 mg/mL, then an exemplary dose for the autoinjector device is 360 mg (1.8 mL of 200 mg/mL solution) given as 2 injections weekly, for a total weekly dose of 720 mg. Compared to the 700 mg dose for a typical 70 kg subject estimated in Study 004, this represents a small (approximately 2%) dose adjustment which falls well within the CI of the absolute BA estimate. Overall, Study 004 resulted in a precise estimate of the absolute BA of lecanemab subcutaneous administration compared to reference intravenous infusion administration. These results, with a slight adjustment to account for the specifications and requirements of the autoinjector device planned for eventual subcutaneous administration, support a proposed fixed lecanemab dose of 720 mg SC administered weekly. In Study 004, 12 TEAEs were reported in 30 subjects receiving the intravenous formulation, and 10 in 29 subjects receiving the subcutaneous formulation. No serious adverse events (SAEs) were reported in either treatment arm, and only one TEAE leading to interruption of study drug was reported and this was in the intravenous treatment arm. Infusion related reactions were reported in 10 subjects; all were mild (3) or moderate (7). Among the subjects who received the subcutaneous formulation, local pain, tenderness and induration occurred in one subject each, and injection site redness was reported in 6 subjects. All injection reactions were considered mild or moderate, and resolved during the course of the study. Regarding general (systemic) disorders, there were no cases of pyrexia, fatigue or chills in subjects receiving the subcutaneous formulation. One subject in the subcutaneous treatment arm presented with unspecific complaints that were reported as injection related reaction. Four subjects (2 in the intravenous arm and 2 in the subcutaneous arm) had confirmed positive ADA, with titers ranging from 16 to 32. One subject in the intravenous arm was confirmed ADA positive at predose and stayed positive until last sampling day (per the clinical site, the subject was not on any prior immunotherapy). None of the 4 subjects with ADA had neutralizing antibodies. In general, both routes of administration were considered well tolerated and no unexpected safety findings were observed in either treatment arm. Attorney Docket No.08061.0062-00304 Example 5. Bioequivalence of Subcutaneously Administered Doses (Study 005) In addition to the drug-in-vial presentation (SC Vial) used in the bioavailability assessment of Study 004 (above), a second SC administration dosing presentation was developed. This presentation, an Autoinjector (AI) Device, was developed and initially tested in a bioequivalence (BE) study (Study BAN2401-A001-005 [Study 005]). Study 005 was a single-center, randomized, open- label, parallel-group study that was conducted in healthy subjects to demonstrate the bioequivalence (BE) of lecanemab following a single fixed dose administered subcutaneously from vial (vial/syringe treatment group) and via an autoinjector (autoinjector treatment group). The study consisted of 2 phases: Prerandomization and Randomization. The Prerandomization Phase consisted of a 20-day Screening Period followed by a 1-day Baseline Period. The Randomization Phase consisted of a 1-day Treatment Period, and a Follow-up Period of 49 days. Study treatment took place on day 1 after subject study eligibility had been confirmed and baseline assessments were conducted.160 subjects were randomized in a 1:1 ratio to 1 of 2 treatment groups (vial/syringe or autoinjector) with matching gender and body weight (±20%): - Vial/Syringe treatment group subjects received 720 mg SC lecanemab administered in the lower abdomen from vials (2 consecutive injections of 1.8 mL), and - Autoinjector treatment group subjects received 720 mg SC lecanemab administered in the lower abdomen via autoinjectors (2 consecutive injections of 1.8 mL). Lecanemab was administered by a healthcare professional (HCP) in both treatment groups. Serum concentrations of lecanemab were measured at predetermined time points. On Day 50, a final follow-up visit occurred on the last day of pharmacokinetic (PK) sample collection. - Subjects were eligible for participation in the study if they met all of the following inclusion criteria: - Nonsmoking, male or female, age ≥18 years and ≤65 years at the time of informed consent. To be considered nonsmokers, subjects must have discontinued smoking for at least 4 weeks before dosing. Body Mass Index (BMI) ≥18 and <30 kg/m2 at screening. The primary objective of the study was to demonstrate BE of a single fixed dose administered from the SC Vial and from the AI Device. The secondary objective was to demonstrate safety, tolerability, and immunogenicity of doses administered according to these presentations. Absolute BA of lecanemab SC administration established in Study 004 was used to identify a 720 mg QW dose that was compatible with the specifications of the AI Device in development. A dosing regimen of 720 mg QW [2 AI Devices] was predicted to result in lecanemab Attorney Docket No.08061.0062-00304 exposure (area under the curve at steady state [AUCss]) equivalent to that following IV LEC10-BW to enable bridging of safety and efficacy data from studies conducted with the IV formulation. Mean (SD) serum concentration-time curves of lecanemab are presented on a linear and semi-logarithmic scale in Figure 33. In Figure 33, Mean (±SD) Serum Lecanemab Concentration- Time Profiles Following 720 mg Subcutaneous Lecanemab Injection With Vial/Syringe or 720 mg Subcutaneous Lecanemab Injection With an Autoinjector (AI) – PK Analyses Set (Presented on a Linear [A] and Semi-Logarithmic [B] Scale). Descriptive statistics for lecanemab serum concentrations after Vial/Syringe administration (720 mg) and Autoinjector administration (720 mg) are presented in Table 14. Table 14. Descriptive statistics for lecanemab serum concentrations

summarized in Table 15, showing subcutaneous lecanemab injection with vial and syringe (Vial/Syringe) or 720 mg subcutaneous lecanemab injection with an autoinjector (PK analysis set) Table 15. Pharmokinetic parameters of lecanemab in serum after administration of 720 mg.

Attorney Docket No.08061.0062-00304

area under the concentration-time curve from zero up to infinite time, Cmax = maximum observed serum concentration, CV = coefficient of variation, Max = maximum, Min = minimum, SD = standard deviation, t½ = terminal elimination phase half-life, tmax = median time to maximum concentration. Boxplots for Cmax, AUC(0-inf), and AUC(0-t) of lecanemab in serum after 720 mg subcutaneous lecanemab injection with a vial and syringe (Vial/Syringe) or 720 mg subcutaneous lecanemab injection with an autoinjector are presented in Figure 36, Figure 37, and Figure 38, respectively. Figure 34 shows boxplots for C_max of lecanemab in serum after 720 mg subcutaneous lecanemab injection with vial and syringe (Vial/Syringe) or 720 mg subcutaneous lecanemab injection with an autoinjector (AI) (PK analysis set). Figure 35 shows boxplots for AUC(_0-inf) of lecanemab in serum after 720 mg subcutaneous lecanemab injection with vial and syringe (Vial/Syringe) or 720 mg subcutaneous lecanemab injection with an autoinjector (AI) (PK analysis set). Attorney Docket No.08061.0062-00304 Figure 36 shows boxplots for AUC(0-t) of lecanemab in serum after 720 mg subcutaneous lecanemab injection with vial and syringe (Vial/Syringe) or 720 mg subcutaneous lecanemab injection with an autoinjector (AI) (PK analysis set). After subcutaneous dosing, the mean maximum serum concentration (Cmax) was reached at approximately 96 hours in both the Vial/Syringe and Autoinjector treatment groups. The mean Cmax in the Vial/Syringe treatment group (53.7 μg/mL) was lower than the mean Cmax of the Autoinjector treatment group (67.4 μg/mL). The mean AUC(0-t) and AUC(0-inf) was lower in the Vial/Syringe treatment group (17,100 and 17,500 ug ^h/mL, respectively) compared to the Autoinjector treatment group (20,600 and 20,900 ug ^h/mL, respectively). The half-life of lecanemab was approximately 7 days in both treatment groups. Results from the study indicate that administration from the AI Device led to higher exposure compared to the SC Vial. AI Device administration resulted in approximately 25% higher Cmax and 20% higher AUC compared to the SC Vial administration. Evaluation of Bioequivalence (BE) Cmax, AUC(0-inf), and AUC(0-t) of lecanemab were compared between single 720 mg doses administered from either a vial/syringe (reference) and via an autoinjector (test) using a linear model of logarithmically transformed values (Table 16). Autoinjector administration resulted in approximately 25% higher Cmax and 20% higher AUC compared to administration with vial/syringe. The upper 90% CI of the difference in geometric means were outside the standard reference of 125%, therefore BE of the autoinjector and vial/syringe administrations was not demonstrated. Table 16. Statistical analysis of the natural log-transformed AUC and Cmax values of lecanemab

In Table 16, AUC(0-inf) = area under the concentration-time curve from time zero to time extrapolated to infinity, AUC(0-t) = area under the concentration-time curve from time zero to time of last quantifiable concentration, CI = confidence interval, Cmax = maximum observed drug concentration, GeoMean = geometric mean. a: Geometric Mean based on Least Squares Mean. b: Ratio (%) = (Geometric Mean (Test)/Geometric Mean (Ref)) x 100. c: 90% Confidence Interval. BE of the AI Device and SC Vial administrations was not demonstrated because the upper 90% CI of the difference in geometric least square means was outside the standard reference of 125%. Attorney Docket No.08061.0062-00304 Overall, the exposure to lecanemab was higher in the AI treatment group compared to the Vial/Syringe treatment group. The AI administration resulted in approximately 25% higher C_max and 20% higher AUC compared to vial/syringe administration. Bioequivalence of the autoinjector and vial/syringe administration was not demonstrated (because the upper 90% CI of the difference in geometric means was outside the standard reference of 125%). The overall incidence of treatment emergent adverse events (TEAEs) was lower in subjects that received subcutaneous lecanemab vial/syringe compared to AI. All TEAEs were mild to moderate. The most common treatment-related TEAEs (≥5%) occurring in both treatment groups were injection site erythema/redness (35.6% overall), pain (10.6% overall), and headache (6.3% overall). There were no TEAEs that led to discontinuation of the subject from the study. There were no clinically significant changes in laboratory test findings, ECGs, or vital signs reported in this study. There were no deaths or serious adverse effects (SAEs) reported in this study. The incidence of local injection site rejections was lower in the vial/syringe treatment group. All injection site reactions were mild to moderate, and no severe rejections were reported. The incidence of system reactions was low and similar between treatment groups, and all were rated Grade 1 in severity. Treatment-emergent anti-drug antibody (ADA) incidences were similar and low at 7.5% each in both treatment groups and at 2.5% for neutralizing antibodies (NAb’s) in vial/syringe versus 0% for autoinjector. Overall, the titers for ADA and NAb were low. Example 6. Core Study (Study 301) and Subcutaneous Substudies 1. Background BAN2401-G000-301 (Study 301) is described above in Example 1. Briefly, Study 301 was an 18-month treatment (Core Study), multicenter, double blind, placebo controlled, parallel-group study in subjects with EAD (MCI due to AD with intermediate likelihood/prodromal AD or mild AD dementia) with confirmed amyloid pathology indicated by positive amyloid load. At the end of the Core Study, subjects who completed 18 months of study drug treatment had the option of enrolling into the open-label Extension Phase, provided they met the inclusion/exclusion criteria. An optional substudy to the Extension Phase will explore the subcutaneous administration of BAN2401. Subcutaneous BAN2401 will be administered by a Healthcare Professional (HCP) using a vial and syringe, in subjects who complete the Core study (which can include subjects previously treated only with placebo before starting subcutaneous BAN2401 in the subcutaneous vial substudy during the Extension Phase and subjects previously treated with intravenous BAN2401). Subjects located in the US and Japan, who are eligible for entry to the Extension Phase will also be eligible to participate in the subcutaneous vial substudy, if it aligns with the recruitment window for this Attorney Docket No.08061.0062-00304 substudy. If these subjects begin open-label treatment directly on the subcutaneous vial substudy upon completion of the Core Study, they must agree to participate in or continue to participate in the amyloid PET substudy. Subjects can also enroll into the subcutaneous vial substudy after 6 months of intravenous treatment in the Extension Phase, but these subjects are not required to take part in the amyloid PET substudy but those who are participating in the amyloid PET substudy may continue in the amyloid PET substudy per the regular schedule of assessments. Subjects are not permitted to begin the subcutaneous vial substudy at any other point during the Extension Phase. The subcutaneous vial substudy is optional as subjects who wish to continue on intravenous treatment during the Extension Phase may choose to do so. In addition, de novo subjects (i.e., subjects who have not participated in the Core Study) from select sites in the US and Japan (based on feasibility) will also be enrolled to participate in the subcutaneous vial substudy such that up to approximately 50 BAN2401-naïve subjects (i.e., de novo subjects plus newly-treated Core placebo subjects) will participate in the subcutaneous vial substudy. These de novo subjects will meet specified inclusion and exclusion criteria (including consent to participate in the amyloid PET substudy) and undertake screening procedures before enrollment at Visit 42. Clinical evaluations in the Screening Period for de novo subjects will be organized into 2 stages. Stage 1 will include all assessments with the exception of amyloid PET, which will be performed during Stage 2. During the course of the subcutaneous vial substudy, individual requests to transition to intravenous treatment can be discussed with the Medical Monitor on a case-by-case basis. The subcutaneous vial substudy (including the de novo cohort) will end as soon as possible after 12 months of treatment. Subjects in the subcutaneous vial substudy will be requested to transition to an alternate administration as soon as possible after 12 months. They will either revert to intravenous administration (excluding de novo subjects) or enroll in the optional AI (autoinjector) substudy, where they will be able to continue to receive weekly subcutaneous administrations on site if preferred. Once a subject has reverted to intravenous administration or enrolled in the optional AI substudy, they cannot revert to subcutaneous vial administration. An optional subcutaneous AI substudy will be conducted to explore weekly subcutaneous administration of BAN2401 using an AI device (the subcutaneous AI substudy). Subjects choosing to enroll into this substudy must have completed at least 6 months of BAN2401 treatment intravenously or at least 12 months subcutaneously. This minimum 6 months of BAN2401 intravenous treatment can have occurred during the Core Study (with confirmed treatment allocation following Core Study database lock) or have occurred during the Extension Phase. If subjects who are participating in the subcutaneous vial substudy want to enroll into the subcutaneous AI substudy, then they must have also been in the subcutaneous vial substudy for at least 12 months. Eligible subjects can enroll into the Attorney Docket No.08061.0062-00304 subcutaneous AI substudy at any Extension Phase visit. The subcutaneous AI substudy will enroll approximately 300 subjects from the Extension Phase. Subject enrollment will be competitive and capped on a regional/country level, depending on drug supply in each region. Additionally, subjects who have taken part in the subcutaneous vial study will be provided the option to enroll in the subcutaneous AI study after at least 12 months in the subcutaneous vial substudy. Subject enrollment will be based on the need for local data to support regulatory filing and potentially capped on a regional/country level. The subcutaneous AI substudy will evaluate subcutaneous administration using an AI device, which may be administered by a non-HCP (such as the subject, study partner, or a family member) at the investigator’s discretion and only after the required training has been completed. The minimum period of initial AI training for non-HCP users will be 2 weeks and will take place across 2 consecutive study drug administration visits in clinic. If there is no suitable non-HCP to administer study drug using the AI device, study drug administration can be performed by an HCP. Drug accountability of all AI devices must be maintained for all administrations, including in clinic and non-HCP administrations of the AI device. The AI drug accountability data must be collected at each study drug dispensing visit by site staff prior to further study drug dispensation. Drug accountability will be checked by counting the number of used and unused AI devices returned by the subject and compliance will be calculated based on the accountability. Four weeks (± 2 weeks) of study drug can be dispensed for non-HCP administration. The investigator (or delegate) should also review the AI injection technique every 6 months. To continue with non-HCP administration of study drug using the AI device, there must be no concerns with either compliance or AI injection technique. For study visits that contain assessments other than study drug administration (eg, vital signs, prior/concomitant medication assessment, and AE assessment), these assessments must be completed in-clinic. All subjects taking part in this subcutaneous AI substudy will continue with the regular schedule of clinical and cognitive assessments within the Extension Phase. Investigators are to remind subjects to promptly notify the investigator of any AEs or changes to concomitant medications occurring between dispensing visits (i.e., subjects should not wait until the next dispensing visit to notify the site). During the open-label Extension Phase, subjects will receive open-label treatment with BAN2401, as follows: ^ 10 mg/kg IV, biweekly treatment with BAN2401 ^ Or, if participating in the subcutaneous [vial] substudy, weekly subcutaneous injections of 720 mg (composed of 2 consecutive [ie, “back-to-back”] injections of 360 mg [2x1.8 mL of 200 mg/mL SC formulation]) using vial and syringe for at least 12 months, Attorney Docket No.08061.0062-00304 ^ Or, if participating in the subcutaneous [AI] substudy, weekly subcutaneous injections of 720 mg BAN2401, administered as 2 consecutive injections of 360 mg [2x1.8 mL of 400 mg/2 mL SC formulation], transitioning to 500 mg SC AI, composed of 2 consecutive injections of 250 mg [2x1.25mL of 2 x 1.25 mL of 200 mg/mL SC formulation] for AI subjects) ^ Or, if participating in the subcutaneous 360 mg AI substudy, weekly subcutaneous injections of a single 360 mg AI device (1x1.8mL) ^ for up to 4 years, or until BAN2401 is commercially available, or until a positive risk-benefit assessment in this indication is not demonstrated, whichever comes first. Upon approval of BAN2401 in Japan, subjects who meet the approved indication and dosage of BAN2401 will continue in this study as a postmarketing study. Treatment will continue until BAN2401 is commercially available for individual subjects at each study site, at which time the subjects will be switched to commercial BAN2401. For those subjects who seamlessly transition to commercial BAN2401 (including postmarketing part in Japan), the end of the study will be the date of the last study evaluation prior to transitioning to commercial BAN2401 and at which time, all assessments included in Visit 146/Early Termination Visit are to be performed. In Sweden, the Extension Phase will continue for up to 4 years. Subjects who are participating in the subcutaneous AI substudy or the subcutaneous 360 mg AI substudy and wish to continue in it, may do so until either BAN2401 delivered by the subcutaneous route becomes commercially available in their country or its development is discontinued, whichever comes first. Subjects who consented to the amyloid PET, tau PET, and/or CSF substudies during the Core Study may continue these substudy evaluations. Subjects participating in the subcutaneous vial substudy at the beginning of the open-label Extension Phase must be willing to participate or continue participating in the amyloid PET substudy. Subjects participating in the subcutaneous vial substudy after 6 months of open-label intravenous treatment are not required to participate in the amyloid PET substudy, but those who are participating in the amyloid PET substudy may continue in the amyloid PET substudy per the regular schedule of assessments. Subjects who do not participate in the Extension Phase will undergo the 3-month Follow- up Visit. Subjects who participate in the Extension Phase will complete their final Core Visit (Visit 42) and will continue seamlessly into the Extension Phase. The Core Study was considered complete once all subjects (excluding subjects randomized in China) completed 18 months of treatment. Data from the Core Study, excluding data from the subjects randomized in China, was locked, unblinded, and analyzed after all subjects Attorney Docket No.08061.0062-00304 complete 18 months of treatment. Data from the China cohort was locked, unblinded, and analyzed after all subjects randomized in China complete 18 months of treatment. An overview of the study design is presented in Figure 37. Dashed lines (-----) indicate optional substudies to the Extension Phase. AI: autoinjector, IV: intravenous, PET: positron emission tomography, R: Randomization, SC: subcutaneous. a: An additional 15 to 90-day window is permitted if prior approval is obtained from the sponsor. b: All subjects will have follow-up 3 months after their last administration of study drug at either the end of the Core Study (21 months) or at the end of the Extension Phase (69 months) or after Early Discontinuation from either the Core Study or the Extension Phase. The 3 month follow-up visit is not required for any subject who transitions directly from the Extension Phase (icluding postmarketing part in Japan) of the study to commercial BAN2401. For those subjects who seamlessly transition to commercial BAN2401 (including postmarketing part in Japan), the end of the study will be the date of the last study evaluation prior to transitioning to commercial BAN2401 and at which time, all assessments included in Visit 146/ET Visit are to be performed. c: Subjects located in the US and Japan, who are eligible for entry to the Extension Phase will also be eligible to participate in the subcutaneous vial substudy, if it aligns with the recruitment window for this substudy. Subjects that have not yet started the Extension Phase can begin open-label treatment directly on the subcutaneous vial substudy upon completion of the Core Study and must agree to participate in or continue in the amyloid PET substudy. Subjects can also enroll into the subcutaneous vial substudy after 6 months of intravenous treatment in the Extension Phase but these subjects are not required to take part in the amyloid PET substudy but those who are participating in the amyloid PET substudy may continue in the amyloid PET substudy per the regular schedule of assessments. d: At select sites in the US and Japan (based on feasibility), de novo subjects (ie, subjects who did not participate in the Core study) will be enrolled in the subcutaneous vial substudy for a minimum of 6 months before having the option to transition to the subcutaneous AI substudy or being provided the option to be treated with intravenous BAN2401. De novo subjects must agree to participate in the amyloid PET substudy e: Subjects choosing to enroll into the optional subcutaneous autoinjector (AI) substudy must have completed at least 6 months of BAN2401 treatment intravenously or at least 12 months subcutaneously. This minimum 6 months of BAN2401 treatment can have occurred during the Core Study (with confirmed treatment allocation following Core Study database lock) or have occurred during the Extension Phase. Subjects will undergo a transition from 720 mg SC to 500 mg SC (composed of 2 consecutive [ie, "back-to-back" injections using 250mg [2x 1.25 mL of 400mg/2 mL SC formulation] AI devices upon implementation of Protocol Amendment 16. Attorney Docket No.08061.0062-00304 f: An optional subcutaneous 360 mg AI substudy will be conducted to explore weekly subcutaneous administration of BAN2401 using a single 360 mg AI device. Subjects enrolling in this substudy must have previously received BAN2401 by either intravenous administration and/or SC AI administration AND must have completed Visit 82 (Extension Week 79) at a minimum, regardless of previous route of administration. 2. PK Comparability In follow-up to the results from Study 004, and the modeling and simulation analyses summarized herein, which consistently demonstrated that a 720 mg SC weekly dose achieves bioequivalent exposure to 10 mg/kg IV biweekly, further PK comparability of 720 mg SC weekly (composed of 2 consecutive [i.e., “back-to-back”] injections of 360 mg [2x1.8mL of 400 mg/2 mL SC formulation]), with a transition to 500 mg SC weekly (composed of 2 consecutive injections of 250 mg [2s1.25 mL of 200 mg/mL SC formulation, and 10 mg/kg IV biweekly will be evaluated using data from the subcutaneous vial substudy via a population modeling approach. PK data supporting the modeling will be obtained from approximately 135 subjects who participate in the subcutaneous vial substudy, composed of the following groups of subjects: 1. Subjects who have completed the Core Study and are transitioning into the Extension Phase, switching from intravenous infusion to syringe/vial injection; these subjects must also enter the amyloid PET substudy. 2. BAN2401-naïve (i.e., newly treated Core Placebo or de novo subjects who have not participated in the Core Study). These subjects will be recruited to enroll directly into the subcutaneous vial substudy at Visit 42; these subjects must enter the amyloid PET substudy. 3. Subjects switching from intravenous to subcutaneous syringe/vial injection after completing at least 6 months of intravenous administration in the Extension Phase. These subjects are not required to enter the amyloid PET substudy, though if they are already participating in it, they may continue. 3. Objectives of the Extension Study The primary objectives of the Extension Study are to evaluate the long term safety and tolerability of BAN2401 in subjects with EAD in the Extension Phase and to evaluate whether the long-term effects of BAN2401 as measured by the CDR-SB at the end of the Core Study is maintained over time in the Extension Phase. The Exploratory Objectives of the Extension Study are as follows: To evaluate the long term effects of BAN2401 on measurements of cognitive function and biomarkers (e.g., ADAS-Cog14, ADCOMS, ADCS MCI ADL, modified iADRS, EQ-5D-5L, QOL- AD, Zarit Burden Interview, amyloid PET, tau PET, blood and CSF biomarkers (neurogranin [CSF Attorney Docket No.08061.0062-00304 only], NFL, Aβ[142], Aβ[1-40], plasma Aβ42/40 ratio, t-tau, and p-tau [including, but not limited to p-tau181, p-tau217, the ratio of p-tau181/np-tau181, and/or the ratio of p-tau217/np-tau217), and vMRI biomarkers after the Core Study and over time in the Extension Phase. Measurements obtained at the end of the Core Study will be monitored over time in the Extension Phase to evaluate whether the effects are maintained over time. To explore the long-term effects of BAN2401 on conversion from amyloid PET positive to amyloid PET negative by visual read, SUVR, and Centiloids at each visit assessed in subjects with EAD in the Extension Phase. To explore the relationship between clinical changes (CDR-SB, ADAS-Cog14, ADCOMS, ADCS MCI-ADL, and modified iADRS) and changes in biomarkers of AD pathology (including but not limited to, amyloid PET, tau PET, blood and CSF biomarkers [Aβ[1-42], Aβ[1-40], plasma Aβ42/Aβ40 ratio, neurogranin, NFL, t-tau, and p-tau] [including, but not limited to p- tau181]). To evaluate patterns of resource utilization and associated costs of care for subjects with EAD and their study partners, using medical claims data. 4. Additional Objectives of the Subcutaneous Substudies The subcutaneous vial substudy (US and Japan only) and subcutaneous AI substudy will have the following additional objectives: a. Additional Primary Objectives of the Subcutaneous Substudies The subcutaneous vial substudy in select studies (based on feasibility) and subcutaneous AI substudy will have the following additional objectives: To evaluate the safety and tolerability of BAN2401 in subjects with EAD, when BAN2401 is administered subcutaneously over the Extension Phase subcutaneous treatment period in all subjects from the subcutaneous vial and AI substudies. To evaluate the PK of BAN2401 in subjects with EAD, when BAN2401 is administered subcutaneously over the Extension Phase subcutaneous treatment period in all subjects from the subcutaneous vial and AI substudies. The subcutaneous 360 mg AI substudy in select countries (based on feasibility) will have the Primary Objectives: to evaluate the safety and tolerability of BAN2401, when administered subcutaneously as a subcutaneous 360 mg AI dosing regimen over the Extension Phase subcutaneous 360 mg AI treatment period. In addition, to explore the PK and immunogenicity of BAN2401, when administered subcutaneously as a subcutaneous 360 mg AI dosing regimen over the Extension Phase subcutaneous 360 mg AI treatment period. Attorney Docket No.08061.0062-00304 b. Secondary Objectives of the Subcutaneous Substudies The subcutaneous vial substudy (US and Japan only) and subcutaneous AI substudy will have the following secondary objectives: To explore the immunogenicity of BAN2401 in subjects with EAD, when BAN2401 is administered subcutaneously over the Extension Phase subcutaneous treatment period in all subjects from the subcutaneous vial and AI substudies. To evaluate the effect of BAN2401 on amyloid PET in subjects with EAD, when BAN2401 is administered subcutaneously over the Extension Phase subcutaneous treatment period in all subjects from the subcutaneous vial and AI substudies who also participated in the amyloid PET substudy. To evaluate the effect of BAN2401 on plasma biomarkers (i.e., p-tau181) in subjects with EAD, when BAN2401 is administered subcutaneously over the Extension Phase subcutaneous treatment period in all subjects from the subcutaneous vial and AI substudies. For administration of a subcutaneous 360 mg AI dose: to evaluate the PK of BAN2401 when administered subcutaneously as a subcutaneous 360 mg AI dosing regimen over the Extension Phase subcutaneous 360 mg AI treatment period. c. Exploratory Objectives of the Subcutaneous Substudies An exploratory objective of the subcutaneous substudies is to explore compliance of subcutaneous administration of BAN2401 using an AI device when administered by a non-HCP in the AI substudy. 5. Eligibility Criteria a. Inclusion Criteria Subjects who have completed the Core Study (except de novo subjects). Must continue to have a study partner who is willing and able to provide follow-up information on the subject throughout the course of the Extension Phase. The study partner must provide separate written informed consent for the Extension Phase. Study partners must continue to participate in person for visits where clinical assessment of CDR (global and CDR-SB), EQ-5D-5L, QOL-AD, ADCS MCI-ADL, and Zarit Burden Interview take place. Provide written informed consent for the Extension Phase. If a subject lacks capacity to consent in the investigator's opinion, the subject's assent should be obtained, if required and in accordance with local laws, regulations and customs, plus the written informed consent of a legal representative should be obtained (capacity to consent and definition of legal representative should be determined in accordance with applicable local laws and regulations). In countries where local laws, Attorney Docket No.08061.0062-00304 regulations, and customs do not permit subjects who lack capacity to consent to participate in this study (e.g., Germany and Spain), they will not be enrolled. Willing and able to comply with all aspects of the protocol. b. Additional Inclusion Criteria for the Subcutaneous Vial Substudy In the US and Japan only, the following additional inclusion criteria will apply: Subjects enrolling into the subcutaneous vial substudy at Extension Phase Week 1, must be willing to participate, or continue participating in the amyloid PET substudy. This criterion includes de novo subjects who must be willing to participate in the amyloid PET substudy. All subjects must have an amyloid PET scan within 4 weeks before starting subcutaneous BAN2401. Subjects do not need to have participated in the Core Study amyloid PET substudy. Subjects enrolling into the subcutaneous vial substudy after 6 months of intravenous treatment in the Extension Phase are not required to take part in the amyloid PET substudy, but those who are participating in the amyloid PET substudy may continue in the amyloid PET substudy per the regular schedule of assessments. For de novo subjects (to be recruited at select sites in the US and Japan, based on feasibility) enrolling directly into the Extension Phase at the subcutaneous vial substudy Visit 42 (ie, did not participate in the Core Study), the following additional inclusion criteria will also apply: Must be willing to participate in the amyloid PET substudy. All subjects must have an amyloid PET scan within 4 weeks before starting subcutaneous BAN2401. A documented diagnosis of Early AD, MCI due to AD, or Mild AD A CDR global score of 0.5 or 1 and a CDR Memory Box score of 0.5 or greater at Screening MMSE score ≥22 and ≤30 at Screening Positive biomarker for brain amyloid pathology as indicated by PET assessment of imaging agent uptake into brain Male or female subjects aged ≥50 and ≤90 years, at the time of informed consent If receiving an approved AD treatment, such as AChEIs, or memantine, or both for AD, must be on a stable dose for at least 12 weeks before Screening. Treatment-naïve subjects for AD medications can be enrolled into into the substudy. Unless otherwise stated, subjects must have been on stable doses of all other (ie, non-AD-related) permitted concomitant medications for at least 4 weeks before Screening. Attorney Docket No.08061.0062-00304 c. Additional Inclusion Criteria for the Subcutaneous AI Substudy The subcutaneous AI substudy has the following additional inclusion criterion: Subjects enrolling into the subcutaneous AI substudy must have had at least 6 months exposure to BAN240110 mg/kg IV (either confirmed BAN2401 IV treatment allocation in the Core Study or at least 6 months exposure in the Extension Phase) or at least 12 months exposure of BAN2401720 mg SC weekly (composed of 2 consecutive [ie, “back-to-back”] injections of 360 mg [2x1.8mL of 400 mg/2 mL SC formulation] as part of the subcutaneous vial substudy (applicable to all subjects in the subcutaneous vial study, including de novo subjects). Subjects enrolling into the subcutaneous 360 mg AI substudy must have previously received BAN2401 by either intravenous administration and/or SC AI administration AND must have completed Visit 82 (Extension Week 79) at a minimum, regardless of previous route of administration. d. Exclusion Criteria The following subjects are excluded from participation in the Extension Phase study: Subjects who discontinued early from the Core Study. Females of childbearing potential who: Do not agree to use a highly effective method of contraception throughout the entire study period and for 28 days after study drug discontinuation, which includes any of the following: total abstinence (if it is their preferred and usual lifestyle) an intrauterine device or IUS a contraceptive implant an oral contraceptive (with additional barrier method) (Subject must be on a stable dose of the same oral contraceptive product for at least 28 days before dosing and throughout the study and for 28 days after study drug discontinuation.) have a vasectomized partner with confirmed azoospermia. For sites outside of the EU and UK, it is permissible that if a highly effective method of contraception is not appropriate or acceptable to the subject, then the subject must agree to use a medically acceptable method of contraception, ie, double-barrier methods of contraception such as latex or synthetic condom plus diaphragm or cervical/vault cap with spermicide. NOTE: All females will be considered to be of childbearing potential unless they are postmenopausal (amenorrheic for at least 12 consecutive months, in the appropriate age group, and Attorney Docket No.08061.0062-00304 without other known or suspected cause) or have been sterilized surgically (ie, bilateral tubal ligation, total hysterectomy, or bilateral oophorectomy, all with surgery at least 1 month before dosing). Subjects who develop the following conditions from the time of Screening for the Core Study to the start of the Extension Phase, or at Screening for those de novo subjects who are enrolling directly into the Extension Phase as part of the subcutaneous vial substudy: Any neurological condition that may be contributing to cognitive impairment above and beyond that caused by the subject’s AD. Any psychiatric diagnosis or symptoms, (eg, hallucinations, major depression, or delusions) that could interfere with study procedures in the subject. Contraindications to MRI scanning, including cardiac pacemaker/defibrillator, ferromagnetic metal implants (eg, in skull and cardiac devices other than those approved as safe for use in MRI scanners). Other significant pathological findings on brain MRI during the Core Study including but not limited to: cerebral contusion, encephalomalacia, aneurysms, vascular malformations, or infective lesions. Evidence of multiple lacunar infarcts or stroke involving a major vascular territory, severe small vessel, or white matter disease; space occupying lesions; or brain tumors will be exclusionary if based on the opinion of the investigator, with consultation of medical monitor, these findings may interfere with the study procedures or safety. Hypersensitivity to BAN2401 or any of the excipients, or to any monoclonal antibody treatment. Any immunological disease which is not adequately controlled, or which requires chronic treatment with immunoglobulins, systemic monoclonal antibodies (or derivatives of monoclonal antibodies), systemic immunosuppressants, or plasmapheresis during the study. Any other clinically significant abnormalities in physical examination, vital signs, laboratory tests, or ECG, which in the opinion of the investigator require further investigation or treatment or which may interfere with study procedures or safety. Malignant neoplasms (except for basal or squamous cell carcinoma in situ of the skin, or localized prostate cancer in male subjects) that are not stably and adequately controlled or which, based on the opinion of the investigator, may interfere with the subject’s safety or participation in the study. Any other medical conditions (eg, cardiac, respiratory, gastrointestinal, renal disease) which are not stably and adequately controlled, or which in the opinion of the investigator(s) could affect the subject’s safety or interfere with the study assessments. Attorney Docket No.08061.0062-00304 Severe visual or hearing impairment that would prevent the subject from performing psychometric tests accurately. Subjects with an answer of “yes” to C-SSRS suicidal ideation Type 4 or 5 at Visit 42 that are not stably and adequately controlled or which, based on the opinion of the investigator, may interfere with the subject’s safety or participation in the study. Subjects who are taking prohibited medications. For de novo subjects enrolling directly into the Extension Phase at the subcutaneous vial substudy Visit 42, the following additional exclusion criteria will also apply: Participation in a clinical study involving any therapeutic monoclonal antibody, protein derived from a monoclonal antibody, immunoglobulin therapy, or vaccine within 6 months before Screening unless it can be documented that the subject was randomized to placebo. Participation in a clinical study involving any anti-amyloid therapies (including any monoclonal antibody therapies and any BACE inhibitor therapies) unless it can be documented that the subject only received placebo Subjects who have any prior exposure to BAN2401 Subjects who were dosed in a clinical study involving any new chemical entities for AD within 6 months prior to Screening unless it can be documented that the subject only received placebo Participated in any other investigational medication or device study in the 8 weeks or 5 half-lives (whichever is longer) of the medication before randomization unless it can be documented that the subject only received placebo Evidence of other clinically significant lesions on brain MRI at Screening that could indicate a dementia diagnosis other than AD. Other significant pathological findings on brain MRI at Screening, including but not limited to: more than 4 microhemorrhages (defined as 10 mm or less at the greatest diameter); a single macrohemorrhage greater than 10 mm at greatest diameter; an area of superficial siderosis; evidence of vasogenic edema; evidence of cerebral contusion, encephalomalacia, aneurysms, vascular malformations, or infective lesions; evidence of multiple lacunar infarcts or stroke involving a major vascular territory, severe small vessel, or white matter disease; space occupying lesions; or brain tumors (however, lesions diagnosed as meningiomas or arachnoid cysts and less than 1 cm at their greatest diameter need not be exclusionary) Planned surgery which requires general anesthesia that would take place during the study. Planned surgery which requires only local anesthesia and which can be undertaken as day case Attorney Docket No.08061.0062-00304 without inpatient stay postoperatively need not result in exclusion if in the opinion of the investigator this operation does not interfere with study procedures and subject safety Severe visual or hearing impairment that would prevent the subject from performing psychometric tests accurately. Known or suspected history of drug or alcohol abuse or dependence within 2 years before Screening or a positive urine drug test at Screening. Subjects who test positive for benzodiazepines or opioids in urine drug testing need not be excluded if in the clinical opinion of the investigator, this is due to the subject taking prior/concomitant medications containing benzodiazepines or opioids for a medical condition and not due to drug abuse History of TIA, stroke, or seizures within 12 months of Screening GDS score greater than or equal to 8 at Screening Hypersensitivity to BAN2401 or any of the excipients, or to any monoclonal antibody treatment Subjects with a bleeding disorder that is not under adequate control (including a platelet count <50,000 or INR >1.5 for subjects who are not on anticoagulant treatment, eg, warfarin). Subjects who are on anticoagulant therapy should have their anticoagulant status optimized and be on a stable dose for 4 weeks before Screening. Subjects who are on anticoagulant therapy are not permitted to participate in CSF assessments. Have thyroid stimulating hormone above normal range. Other tests of thyroid function with results outside the normal range should only be exclusionary if they are considered clinically significant by the investigator. This applies to all subjects whether or not they are taking thyroid supplements. Abnormally low serum vitamin B12 levels for the testing laboratory (if subject is taking vitamin B12 injections, level should be at or above the LLN for the testing laboratory). Levels of Vitamin B12 may be confirmed with reflex testing to include MMA analysis, if available in region. Known to be HIV positive Any other clinically significant abnormalities in physical examination, vital signs, laboratory tests, or ECG at Screening or Baseline which in the opinion of the investigator require further investigation or treatment or which may interfere with study procedures or safety. 6. Study Plan and Design The Extension Phase will be initiated following the Core Study to allow all subjects to receive open label BAN240110 mg/kg IV biweekly for up to 48 months (4 years) or until the drug is commercially available in the country where the subject resides, or the benefit to risk ratio from Attorney Docket No.08061.0062-00304 treatment with BAN2401 is no longer considered favorable, whichever comes first. In Sweden, the Extension Phase will continue for up to 4 years. Upon approval of BAN2401 in Japan, subjects who meet the approved indication and dosage of BAN2401 will continue in this study as a postmarketing study. Treatment will continue until BAN2401 is commercially available for individual subjects at each study site, at which time the subjects will be switched to commercial BAN2401. For those subjects who seamlessly transition to commercial BAN2401 (including postmarketing part in Japan), the end of the study will be the date of the last study evaluation prior to transitioning to commercial BAN2401 and at which time, all assessments included in Visit 146/Early Termination Visit are to be performed. Extension Phase subjects will remain blinded to Core treatment until the blind for the Core Study has been broken after Core Study database lock. A substudy to the Extension Phase will be conducted in the US and Japan to explore the subcutaneous administration of BAN2401. Subcutaneous BAN2401 will be administered by a Healthcare Professional (HCP) using a vial and syringe, in subjects who complete the Core study (which can include subjects previously treated only with placebo before starting subcutaneous BAN2401 in the subcutaneous vial substudy during the Extension Phase and subjects previously treated with intravenous BAN2401). Subjects located in the US and Japan, who are eligible for entry to the Extension Phase will also be eligible to participate in the subcutaneous vial substudy, if it aligns with the recruitment window for this substudy. Subjects that have not yet started the Extension Phase can begin open-label treatment directly on the subcutaneous vial substudy upon completion of the Core Study and must agree to participate in or continue in the amyloid PET substudy. Subjects can also enroll into the subcutaneous vial substudy after 6 months of intravenous treatment in the Extension Phase but these subjects are not required to take part in the amyloid PET substudy but those who are participating in the amyloid PET substudy may continue in the amyloid PET substudy per the regular schedule of assessments. Subjects are not permitted to begin the subcutaneous vial substudy at any other point during the Extension Phase. The subcutaneous vial substudy is optional as subjects who wish to continue on intravenous treatment during the Extension Phase may choose to do so. In addition, de novo subjects (i.e., subjects who have not participated in the Core Study) from select sites in the US and Japan (based on feasibility) will also be enrolled to participate in the subcutaneous vial substudy such that up to approximately 50 BAN2401-naïve subjects (i.e., de novo subjects plus newly-treated Core placebo subjects) will participate in the subcutaneous vial substudy. These de novo subjects will meet specified inclusion and exclusion criteria (including consent to participate in the amyloid PET substudy) and undertake screening procedures before enrollment at Visit 42. Clinical evaluations in the Screening Period for de novo subjects will be organized into 2 Attorney Docket No.08061.0062-00304 stages. Stage 1 will include all assessments with the exception of amyloid PET, which will be performed during Stage 2. During the course of the subcutaneous vial substudy, individual requests to transition to intravenous treatment can be discussed with the Medical Monitor on a case-by-case basis. The subcutaneous vial substudy (including the de novo cohort) will end as soon as possible after 12 months of treatment. Subjects in the subcutaneous vial substudy will be requested to transition to an alternate administration as soon as possible after 12 months. They will either revert to intravenous administration (excluding de novo subjects) or enroll in the optional AI substudy, where they will be able to continue to receive weekly subcutaneous administrations on site if preferred. Once a subject has reverted to intravenous administration or enrolled in the optional AI substudy, they cannot revert to subcutaneous vial administration. An optional subcutaneous AI substudy will be conducted (in select countries based on feasibility) to explore weekly subcutaneous administration of BAN2401 using an AI device. Subjects enrolling into this substudy must have completed at least 6 months of BAN2401 treatment intravenously or 12 months of treatment subcutaneously. This minimum 6 months of BAN2401 intravenous treatment can have occurred during the Core Study (with confirmed treatment allocation following Core Study database lock) or have occurred during the Extension Phase. If subjects who are participating in the subcutaneous vial substudy want to enroll into the subcutaneous AI substudy, then they must have also been in the subcutaneous vial substudy for at least 12 months. Eligible subjects can enroll into the subcutaneous AI substudy at any Extension Phase visit. The subcutaneous AI substudy will enroll approximately 300 subjects from the Extension Phase. Subject enrollment will be competitive and capped on a regional/country level, depending on drug supply in each region. Additionally, subjects who have taken part in the subcutaneous vial study will be provided the option to enroll in the subcutaneous AI study after at least 12 months in the subcutaneous vial substudy. Subject enrollment will be based on the need for local data to support regulatory filing and potentially capped on a regional/country level. Subjects can enroll into the subcutaneous AI substudy at any visit if the additional substudy-specific inclusion criterion is met. Weekly subcutaneous administration of study drug will use 2 AI devices. Each weekly dose of BAN2401720 mg SC is composed of 2 consecutive (ie, “back-to-back”) injections of 360 mg (2x1.8mL of 400 mg/2 mL SC formulation). An optional subcutaneous 360 mg AI substudy will be conducted in select countries (based on feasibility) to explore weekly subcutaneous administration of BAN2401 using a 360 mg AI device (1x1.8mL). Subjects enrolling in this substudy must have previously received BAN2401 by either intravenous administration and/or SC AI administration and must have completed Visit 82 (Extension Week 79) at a minimum, regardless of previous route of administration. Attorney Docket No.08061.0062-00304 The subcutaneous 360 mg AI substudy will enroll approximately 50 subjects from the Extension Phase to characterize the safety, PK, and immunogenicity of the subcutaneous 360 mg AI regimen. Subject enrollment will be in select countries (based on feasibility) and recruitment will be competitive. Subjects must have received a minimum of at least 18 months of intravenous and/or subcutaneous AI treatment (ie, completed Visit 82 [Extension Week 79]) at a minimum in order to be eligible for the 360mg AI dosing substudy. The subcutaneous AI substudy and the subcutaneous 360 mg AI substudy will both evaluate subcutaneous administration using an AI device, which may be administered by either an HCP or a non-HCP (such as the subject, study partner, or a family member) at the investigator’s discretion and only after the required training has been completed. The minimum period of initial AI training for non-HCP users will be 2 weeks and will take place across 2 consecutive study drug administration visits in clinic. If there is no suitable non-HCP to administer study drug using the AI device, study drug administration can be performed by an HCP. If AI injections are being given at home by a non-HCP, the only other visits at which a subject in the subcutaneous AI substudy is required to attend the clinic are the dispensing AI visits at which vital signs will be measured and AEs and concomitant medications assessed. For the subcutaneous AI substudy, a baseline PD, PK, and antidrug antibody (ADA) blood draw will be taken at entry into the subcutaneous AI substudy. At the first possible opportunity, such as the next AI dispensing visit, blood draws for serum PK are required to be taken predose as well as 2 hours post dose, with a further predose PK blood draw taken at the next weekly AI administration of study drug. At the discretion of the sponsor, it is possible that this additional PK sampling for the AI substudy may not be required for all AI substudy subjects. Subjects will have additional PK draws before the 1st administration of the optimized 500 mg weekly SC dose and predose at 4, 6, 8, and 12 weeks after switching to the subcutaneous 500 mg AI dosing regimen, with a window of ±1 week. For the subcutaneous 360 mg AI substudy, subjects will have additional PK and ADA draws before the 1st administration of the optimized 360 mg SC dose and predose at 4, 6, 8, and 12 weeks (with a window of ±1 week) after switching to the subcutaneous 360 mg AI dosing regimen, and additional PD draws before the first dose administration of the 360 mg weekly SC dose and predose at 12 weeks (±1 week) after switching to the subcutaneous 360 mg AI dosing regimen. Drug accountability of all AI devices must be maintained for all administrations, including in clinic and non-HCP administrations of the AI device. The AI drug accountability data must be collected at each study drug dispensing visit by site staff prior to further study drug dispensation. Drug accountability will be checked by counting the number of used and unused AI devices returned by the subject and compliance will be calculated based on the accountability. Four weeks (± 2 weeks) of study drug can be dispensed for non-HCP administration. The investigator (or delegate) should also Attorney Docket No.08061.0062-00304 review the AI injection technique every 6 months. To continue with non-HCP administration of study drug using the AI device, there must be no concerns with either compliance or AI injection technique. A patient diary will be used to collect data on at home administration. For study visits that contain assessments other than study drug administration (eg, vital signs, prior/concomitant medication assessment, and AE assessment), these assessments must be completed in-clinic. All subjects taking part in this subcutaneous AI substudy will continue with the regular schedule of clinical and cognitive assessments within the Extension Phase. Investigators are to remind subjects to promptly notify the investigator of any AEs or changes to concomitant medications occurring between dispensing visits (i.e., subjects should not wait until the next dispensing visit to notify the site). Any subject who completed the Core Study will have the option to participate in the Extension Phase. After completing their last dose of study drug in the Core Study at Visit 41 and completing all Core Study procedures in Visit 42, subjects enrolling into the Extension will immediately transition to the Extension Phase and will not undergo the 3-month Core Study Follow- up Visit. Subjects participating in the subcutaneous vial substudy will be randomly assigned their injection site, which will be either the abdomen, the thigh or the upper arm, with a fixed 1:1:1 schedule at each enrollment point (Visit 42 or Visit 56). Each consecutive injection should be rotated within the assigned injection site, using both sides of the body if needed. If a change to injection site is required, it must be discussed with the Medical Monitor. All subjects will receive open-label IV BAN240110 mg/kg biweekly during the Extension Phase, unless they are participating in the subcutaneous vial substudy, the subcutaneous AI substudy (in which case, they will receive weekly subcutaneous injection of BAN2401, which is composed of 2 consecutive [i.e., “back-to-back”] injections of 360 mg [2x1.8mL of 400 mg/2 mL SC formulation]), or, if participating in the subcutaneous 360 mg AI substudy (in which case, they will receive weekly subcutaneous injections of a 360 mg AI device (1x1.8mL). Subjects who are participating in the subcutaneous AI substudy and wish to continue in it, may do so until either BAN2401 delivered by the subcutaneous route becomes commercially available in their country or its development is discontinued, whichever comes first. No body-weight adjustment of the dose of subcutaneous BAN2401 is required and all subjects will receive the same volume and dose for each subcutaneous injection, whether administered via vial and syringe, or AI device. All intravenous infusions will take place in the clinic; however, if approved by the sponsor and allowable and conducted according to country and local guidelines, subjects will be offered the option of home infusions for all visits except the 1st Extension Phase visit (Visit 42) and visits where clinical assessments are performed (per the schedule of assessments). However, home infusion for visits with clinical assessments may be permitted under extenuating circumstances only with the Attorney Docket No.08061.0062-00304 approval of the sponsor (eg, during the COVID-19 pandemic; see below for conduct of the study during the COVID-19 pandemic and other extenuating circumstances). Home infusions will be allowed per sponsor approval according to country and local guidelines during the COVID-19 pandemic and following its resolution, where permitted. For subjects in the subcutaneous vial substudy, home injections are permitted in special circumstances (eg, the COVID-19 pandemic) except for the 1st subcutaneous administration. Home injections must be administered by a HCP, after discussion with the medical monitor and only if allowable and conducted according to country and local guidelines. This option should be temporary, with injections in the clinic reinstated as soon as possible. For subjects in the subcutaneous AI substudy or the subcutaneous 360 mg AI substudy, study drug administration can occur at home by a non-HCP after the appropriate training has been conducted at the site. At a minimum the first 2 study drug administrations for the subcuataneous AI substudy or the subcutaneous 360 mg AI substudy must occur in-clinic to allow for the appropriate level of training to have occurred. The administration of the study drug by a non HCP is at the investigator’s discretion at all times and based upon review of AI drug accountability data at each dispensing visit and periodic review of AI use technique. Visits that require additional study assessments, should be conducted in clinic where possible. Under extenuating circumstances (eg, the COVID-19 pandemic) these assessments may be conducted remotely by trained study staff. This option should be temporary with clinic visits being restored as soon as possible. During the Extension Phase, subjects who consented to the amyloid PET, tau PET, and/or CSF substudies during the Core Study may continue these substudy evaluations. If these subjects begin open-label treatment directly on the subcutaneous vial substudy upon completion of the Core Study, they must agree to participate, or continue participating, in the amyloid PET substudy. If subjects enroll into the subcutaneous vial substudy after 6 months of intravenous treatment in the Extension Phase, they are not required to take part in the amyloid PET substudy, but those who are regular schedule of assessments. The Follow-up Visit will take place 3 months after the last dose of study drug. The 3 month Follow-up Visit is not required for any subject who transitions directly from the Extension Phase (including postmarketing part in Japan) of the study to commercial BAN2401. For those subjects who seamlessly transition to commercial BAN2401 (including postmarketing part in Japan), the end of the study will be the date of the last study evaluation prior to transitioning to commercial BAN2401 and at which time, all assessments included in Visit 146/Early Termination Visit are to be performed. Subjects may discontinue from study drug for any reason. Subjects who discontinue the study or study drug must comply with the Early Termination Visit (within 7 days of the decision to Attorney Docket No.08061.0062-00304 discontinue from study drug) and the Follow-up Visit (3 months after the last dose of study drug). The study will end when the last assessment for the last subject has completed the Extension Phase. In the Extension Phase, subjects who discontinue early from study drug will also withdraw from the study. 7. Extension Phase Assessments During the Extension Phase, subjects will receive open-label treatment with BAN2401, as follows: Either 10 mg/kg IV biweekly, Or, if participating in the subcutaneous vial substudy, weekly subcutaneous injections of 720 mg (composed of 2 consecutive [i.e., “back-to-back”] injections of 360 mg [2x1.8 mL of 400 mg/2 mL SC formulation]) using vial and syringe for at least 12 months, Or, if participating in the subcutaneous AI substudy, weekly subcutaneous injections of 720 mg (composed of 2 consecutive [i.e., “back-to-back”] injections using 360 mg AI devices (2x1.8 mL of 200 mg/mL SC formulation), transitioning to 500 mg SC AI, composed of 2 consecutive [ie, “back-to-back”] injections of 250 mg [2x1.25 mL of 200 mg/mL SC formulation] for subjects in the AI substudy. Or, if participating in the subcutaneous 360 mg AI substudy, weekly subcutaneous injections of a 360 mg AI device (1x1.8mL) All Clinical, other safety assessments, and HRQoL assessments will be conducted every 6 months according to the Schedule of Assessments. During the Extension Phase, safety assessments will continue to be monitored and all AEs will be recorded. AEs, including SAEs and study-specific AEs, will be identified, assessed, collected, and reported in the same manner as that of the Core Study. Intracerebral hemorrhages >1 cm should always be classified as an important medical event and reported as SAEs even if they do not meet other serious criteria. For subjects who seamlessly transition to commercial BAN2401 (including postmarketing part in Japan), all AEs (including SAEs) will be followed until the end of the study which will be the date of the last study evaluation prior to transitioning to commercial BAN2401 and at which all assessments included in Visit 146/Early Termination Visit are to be performed. Vital signs will be assessed when study drug is administered both predose and after infusion. Subjects in the subcutaneous vial or AI substudies will have weekly study drug administration. For the subcutaneous vial substudy, vital signs, prior/concomitant medication assessment, and AE assessment must be performed every time study drug is administered. For the subcutaneous AI substudy, subjects are to come into the clinic at every visit at which clinical and cognitive assessments are performed (i.e., approximately every 6 months). At these visits injection Attorney Docket No.08061.0062-00304 technique will also be assessed. At AI dispensing visits, vital signs, prior/concomitant medication assessment, and AE assessment must also be undertaken. For the AI substudy, at the first possible opportunity, such as the next AI dispensing visit, blood draws for serum PK are required to be taken predose as well as 2 hours post dose, with a further predose PK blood draw taken at the next weekly AI administration of study drug. At the discretion of the sponsor, it is possible that this additional PK sampling for the AI substudy may not be required for all AI substudy subjects. Subjects will have additional PK draws before the 1st administration of the optimized 500 mg weekly SC dose and predose at 4, 6, 8, and 12 weeks after switching to the subcutaneous 500 mg AI dosing regimen, with a window of ±1 week. For the subcutaneous 360 mg AI substudy, subjects will have additional PK and ADA draws before the 1st administration of the optimized 360 mg weekly SC dose and predose at 4, 6, 8, and 12 weeks (with a window of ±1 week) after switching to the subcutaneous 360 mg AI dosing regimen, and additional PD draws before the first dose administration of the 360 mg weekly SC dose and predose at 12 weeks (±1 week) after switching to the subcutaneous 360 mg AI dosing regimen, with a window of 1week. Hematology, blood chemistry, and urinalysis values will be monitored every 6 months. All subjects will be assessed using clinical laboratory tests, safety MRIs, vMRIs, amyloid PET assessments (for those who consent to longitudinal amyloid PET substudy assessments in the Core Study), tau PET assessments (for those who consent to the longitudinal tau PET substudy), and CSF sampling (for those who consent to longitudinal CSF substudy assessments in the Core Study). All subjects will follow the same safety MRI schedule as in the Core Study for the first 6 months of treatment in the Extension Phase for ARIA-E monitoring (at 9 weeks, 13 weeks, and 6 months after the start of the Extension Phase). Safety MRIs will be conducted every 6 months thereafter until the end of the Extension Phase. vMRI assessments will be collected following all safety MRI assessments and will be analyzed per the schedule of assessments in the Extension Phase. Clinical assessments will be administered every 6 months in the morning (whenever possible) in the following order: MMSE, CDR, and ADAS-Cog14. All clinical assessments (MMSE, CDR, and ADAS-Cog14) must be completed on the same day. All clinical assessments must be completed in the morning whenever possible, or consistently at approximately the same time of day during the study. The EQ-5D-5L, QOL AD, ADCS MCI-ADL, and Zarit Burden Interview will be administered after the completion of the ADAS-Cog14. Blood for serum PK will be collected at Visit 42, Visit 47, Visit 50, and every 3 months thereafter during the 1st year of the Extension Phase, and every 6 months during the 2nd, 3rd, and 4th years of the Extension Phase, at the Early Termination Visit when applicable, and at the Follow up Visit that takes place 3 months after the last dose of study drug. Subjects participating in Attorney Docket No.08061.0062-00304 the subcutaneous vial substudy will require additional blood samples to be taken for serum PK as per the Schedule of Assessments. Amyloid PET will be collected for those who consent to the longitudinal amyloid PET substudy in the Core Study at 30, 42, 56, and 68 months in the Extension Phase (12, 24 , 36, and 48 months after the start of the Extension Phase), while CSF will be collected for those who consent to the longitudinal CSF substudy in the Core Study at 30, 42, 56, and 68 months in the Extension Phase (12, 24, 36, and 48 months after the start of the Extension Phase). Tau PET will be collected for those who consent to the longitudinal tau PET substudy in the Core Study at 30, 42, 56, and 68 months in the Extension Phase (12, 24, 36, and 48 months after the start of the Extension Phase). In the subcutaneous vial substudy, amyloid PET will be collected as below for each group of subjects: Subjects who have completed the Core Study and are transitioning into the Extension Phase, switching from intravenous infusion to syringe/vial injection; these subjects must also enter the amyloid PET substudy. De novo subjects who have not participated in the Core Study must enter the amyloid PET substudy. Subjects switching from intravenous to subcutaneous syringe/vial injection after completing at least 6 months of intravenous administration in the Extension Phase. These subjects are not required to enter the amyloid PET substudy, though if they are already participating in it, they may continue. If requested by the principal investigator (PI), subjects in the subcutaneous vial (excluding de novo subjects) or subcutaneous AI substudies (including the subcutaneous 360 mg AI substudy) may revert to biweekly intravenous administration of BAN2401 following approval by the Medical Monitor. In this case, a blood sample for PK, PD, and ADA will be collected and weight measured before reverting to intravenous infusion, and the subject must remain on biweekly intravenous administration of BAN2401 for the remainder of the Extension Phase (BAN240110 mg/kg IV biweekly for up to 48 months [4 years] or until the drug is commercially available in the country where the subject resides, or the benefit to risk ratio from treatment with BAN2401 is no longer considered favorable, whichever comes first). In Sweden, the Extension Phase will continue for 4 years. All subjects taking part in the subcutaneous AI substudy or the subcutaneous 360 mg AI substudy will continue with the regular schedule of clinical and cognitive assessments within the Extension Phase. Attorney Docket No.08061.0062-00304 In the US only, subjects and study partners may consent to the optional medical claims substudy at any phase of the study (Core Study or Extension Phase). All participants in the substudy will be requested to sign an additional informed consent for the medical claims substudy. A Follow-up Visit will take place 3-months after the last dose of study drug. Subjects may withdraw from the study or discontinue study drug for any reason during the Extension Phase. Subjects who withdraw from the study or discontinue study drug early must comply with the Early Termination Visit (within 7 days of the decision to discontinue from study drug) and the Follow-up Visit (3-months after the last dose of study drug) and may also have unscheduled visits for safety assessments when applicable. In the Extension Phase, subjects who discontinue study drug will not be required to return for each scheduled visit when clinical efficacy assessments are conducted, which means that subjects who discontinue early from study drug during the Extension Phase will also withdraw from the study. The study will end when the last assessment for the last subject of the Extension has concluded. Actions required for subjects with ARIA-H, ARIA-E, or both ARIA-H and ARIA-E during the Extension Phase will follow the same study drug action and required Follow-up Safety Visits (with MRI as applicable). 8. Number of Subjects The Extension Phase will be initiated following the Core Study to allow all subjects to receive open label BAN240110 mg/kg IV biweekly for up to 48 months (4 years) or until the drug is commercially available in the country where the subject resides, or the benefit to risk ratio from treatment with BAN2401 is no longer considered favorable, whichever comes first. In Sweden, the Extension Phase will continue for up to 4 years. For the subcutaneous vial substudy, recruitment will be limited to ensure availability of sufficient drug supplies for the duration of the substudy. Approximately 50 BAN2401-naïve subjects will be enrolled in this substudy to assess PD comparability. To enable this comparison, the substudy will be expanded at select sites in the US and Japan (based on feasibility) to include subjects who did not participate in the Core study (referred to as de novo subjects). Therefore, there will be 2 groups of BAN2401-naïve subjects participating in the subcutaneous vial substudy: newly-treated Core placebo subjects and de novo subjects. De novo subjects will be recruited to enroll directly into the subcutaneous vial substudy at Visit 42. In addition to the BAN2401-naïve subjects, there will be approximately 85 subjects participating in the subcutaneous vial substudy who will have been treated with intravenous BAN2401 either in the Core study or in the Extension Phase. Therefore, the subcutaneous vial substudy will have a total sample size of approximately 135 subjects, which is expected to be sufficient to characterize the PK profile of subcutaneous BAN2401, and with the Attorney Docket No.08061.0062-00304 addition of subjects in the AI substudy is expected to be sufficient to characterize the safety profile of subcutaneous BAN2401. The subcutaneous AI substudy will enroll approximately 300 subjects from the Extension Phase. Subject enrollment will be competitive and capped on a regional/country level, depending on drug supply in each region. Additionally, subjects who have taken part in the subcutaneous vial study will be provided the option to enroll in the subcutaneous AI study after at least 12 months in the subcutaneous vial substudy. Subject enrollment will be based on the need for local data to support regulatory filing and potentially capped on a regional/country level. The subcutaneous 360 mg AI substudy will enroll approximately 50 subjects following at least 18 months of intravenous treatment in the Extension Phase, to characterize the safety and immunogenicity of the subcutaneous 360 mg AI regimen. 9. Study Drug Supplies A single dose of BAN2401, 10 mg/kg IV biweekly will be administered to all subjects in the Extension Phase, except those participating in the subcutaneous vial substudy. For those participating in the subcutaneous vial substudy, BAN2401 will be provided in 2 mL vials of 400 mg BAN2401. Two vials will be provided for each weekly dose. Each weekly dose of BAN2401720 mg SC is composed of 2 consecutive (i.e., “back-to-back”) injections of 360 mg (2x1.8mL of 400 mg/2 mL SC formulation) each of which should be administered by an HCP into the abdomen, thigh, or upper arm, as assigned by the IxRS system, rotating within the assigned injection site in order to minimize pain, bruising or swelling. BAN2401 for subcutaneous administration should be drawn up into single use polypropylene syringes immediately before use and administered using a 25G or similar SC needle over a period of approximately 15 seconds. For subjects participating in the subcutaneous AI substudy and subcutaneous 360 mg AI substudy, 4 weeks (± 2 weeks) of study drug can be dispensed for non-HCP administration. The investigator (or delegate) should also review the AI injection technique every 6 months. To continue with non-HCP administration of study drug using the AI device, there must be no concerns with either compliance or AI injection technique. A patient diary will be used to collect data on at home administration. 10. Removal of Subjects from Therapy or Assessment Subjects who discontinue from treatment during the Extension Phase will also withdraw from the study, and will have a follow-up visit 3 months after the last dose of study drug. Safety-related criteria for discontinuation of study drug are as follows: Attorney Docket No.08061.0062-00304 Infusion or injection reactions (Table 22) associated with administration of study drug, of Grade 3 severity or above (as defined in the NCI-CTCAE or FDA guidance [Toxicity Grading Scale for Healthy Adult and Adolescent Volunteers Enrolled in Preventive Vaccine Clinical Trials], respectively) that do not lessen or resolve with treatment. Table 22. Table for Assessing Severity of Injection Reactions Reaction to Mild (Grade 1) Moderate Severe Potentially Life Injectable Product (Grade 2) (Grade 3) Threatening

Clinical features which indicate meningoencephalitis (eg, combination of 1 or more of the following: headache, worsening confusion, neck stiffness, impaired consciousness, focal neurological signs). Hypersensitivity reactions with clinical features of tissue injury (eg, arthritis, glomerulonephritis, mononeuritis multiplex). Subjects who meet any of the above criteria for study drug discontinuation, whether on MRI or otherwise, will be discontinued from the study. If severe ARIA-E is associated with SAE (results in death, is life-threatening, requires inpatient hospitalization or prolongation of hospitalization, results in persistent or significant disability, or important medical event) the drug will be permanently stopped and no re challenge can be considered. Subjects who develop both ARIA-H and ARIA-E that resulted in study drug interruption at any point during the course of the study will permanently discontinue study drug if a 3rd occurrence of either event (ie, ARIA-H or ARIA-E) meets the criteria for study drug interruption or discontinuation. Attorney Docket No.08061.0062-00304 11. Treatment Administered and Identity of Investigational Products All subjects will receive BAN240110 mg/kg IV biweekly dose, or 720 mg SC weekly, or 360 mg SC weekly during the Extension Phase. Each weekly dose of BAN2401720 mg SC is composed of 2 consecutive (i.e., “back-to-back”) injections of 360 mg (2x1.8mL of 400 mg/2 mL SC formulation). Each weekly dose of BAN2401360 mg SC is composed of one injection of 360 mg (1x1.8 mL of 400 mg/2mL SC formulation). BAN2401 is a humanized IgG1 monoclonal antibody that binds to soluble Aβ aggregates. BAN2401 is manufactured at Biogen, RTP, under contract to Eisai. The intravenous drug product contains 100 mg/mL BAN2401 and is supplied as a sterile aqueous solution containing 100 mg/mL BAN2401, 50 mmol/L citrate, 350 mmol/L arginine, 0.05% polysorbate 80, pH 5.0, in glass vials containing 5 mL solution or supplied in a citrate-free formulation as a sterile aqueous solution containing 100 mg/mL BAN2401, 25 mmol/L histidine, 200 mmol/L arginine, 0.05% polysorbate 80, pH 5.0, in glass vials containing 5 mL solution. Study drug (intravenous) will be packaged such that there are 4 vials per kit, and will be dispensed by a pharmacist at each site according to the IxRS. Individual vials will contain a tear-off label. At the time of dispensing, the tear-off label for each vial used is to be placed in the drug accountability log. The AI device is an automated, disposable 2.25 mL AI device consisting of a housing with a content viewing window, a spring activated mechanism and an integrated needle safety feature. The device contains a 2.25 mL prefilled plastic syringe with a tapered needle, rigid needle cover, and stopper, prefilled with 1.8 mL of 200 mg/mL lecanemab solution. The solution appears as a colorless to pale yellow liquid. The AI is ready to use and does not require any further assembly. The devices will be supplied in cartons, with each carton containing 2 devices for the AI substudy or the subcutaneous 360 mg AI substudy. All infusions will take place in the clinic; however, only if approved by the sponsor and only allowable and conducted according to country and local guidelines, subjects will be offered the option of home infusions for all visits except the 1st Extension Phase visit (Visit 42) and visits where clinical assessments are performed. However, home infusion for visits with clinical assessments (per the schedule of assessments) may be permitted under extenuating circumstances only with the approval of the sponsor (eg, during the COVID-19 pandemic). Home infusions are being implemented as a result of the COVID 19 pandemic to allow subjects who cannot visit clinical sites for various reasons to continue receiving treatment. Home infusions will be allowed per sponsor approval according to country and local guidelines during the COVID 19 pandemic and following its resolution, where permitted. For subjects in the subcutaneous vial substudy, home injections are permitted in special circumstances (eg, the COVID-19 pandemic) except for the first subcutaneous Attorney Docket No.08061.0062-00304 administration. Home injections must be administered by a HCP, after discussion with the medical monitor and only if allowable and conducted according to country and local guidelines. This option should be temporary, with injections in the clinic reinstated as soon as possible. Subjects participating in the subcutaneous vial substudy will receive 2 consecutive SC injections of a fixed dose (720 mg) of BAN2401 on a weekly basis for at least 12 months, administered using a vial and syringe by an HCP. Each weekly dose of BAN2401720 mg SC is composed of 2 consecutive (i.e., “back-to-back”) injections of 360 mg (2x1.8mL of 400 mg/2 mL SC formulation). The study drug for use in the subcutaneous vial substudy will be provided in 2mL vials containing 400 mg of BAN2401 SC manufactured at Biogen, RTP. The drug product will be supplied in a citrate free formulation as a sterile aqueous solution containing 200 mg/mL BAN2401, 25 mmol/L histidine, 200 mmol/L arginine, 0.05% polysorbate 80, pH 5.0, in glass vials containing 2 mL solution. Study drug will be packaged such that there are 2 vials per kit and will be dispensed by a pharmacist or other qualified HCP at each site according to the IxRS. Individual vials will contain a tear-off label that at the time of dispensing, is to be placed in the drug accountability log. Subjects participating in the subcutaneous AI substudy will receive 2 consecutive subcutaneous injections of a fixed dose (720 mg) of BAN2401 on a weekly basis, administered using an AI device. Each weekly dose of BAN2401720 mg SC is composed of 2 consecutive (i.e., “back- to-back”) injections of 360 mg (2x1.8mL of 400 mg/2 mL SC formulation), transitioning to 500 mg SC AI (composed of 2 consecutive ie, “back-to-back,” injections of 250 mg (2x1.25 mL of 200 mg/mL SC formulation)). This will be dispensed in a pack of 2 AI devices. Both AI devices need to be administered for a full dose of study drug. Subjects participating in the subcutaneous 360 mg AI substudy will receive one subcutaneous injections of a fixed dose (360 mg) of BAN2401 on a weekly basis, administered using an AI device. Each weekly dose of BAN2401360 mg SC is composed of one injection of 360 mg (1x1.8mL of 400 mg/2 mL SC formulation). This will be dispensed in a pack of 2 AI devices. For both the AI substudy and the subcutaneous AI maintenance dosing substudy, the AI device can be administered in the abdomen or thigh (for self-administration or if someone else is giving the injection) or the upper arm (if someone else is giving the injection; refer to AI instructions for use for full details). 12. Selection of Doses in the Study PK/PD simulations were conducted to evaluate the effect of differences in lecanemab exposures that are anticipated at low/high body weight extremes on lecanemab efficacy and safety. Attorney Docket No.08061.0062-00304 PK simulations were performed using the PK model for subjects with EAD to explore the impact of body weight on the AUCss of lecanemab when administered as a fixed subcutaneous dose and body-weight based intravenous dose. Key outcomes of the modeling are depicted in Figure 38. In the top plot, lecanemab exposure shows a relative increase with increase in body weight following intravenous dose administration; in contrast, lecanemab exposure shows a relative decrease with increase in body weight for the fixed subcutaneous dose. However, as shown in the lower plot of Figure 38, for a wide range of body weights (approximately 58-90 kg,) lecanemab exposure is equivalent (CI within 80- 125%) for intravenous and subcutaneous administration. The AUCss ratio is higher than 1.25 for subjects with low body weight such as 51 kg (5th percentile of PK analysis set) and is slightly lower than 0.8 for subjects with high body weight such as 99 kg (95th percentile of PK analysis set). In addition to analyses undertaken to further explore effect of body weight on lecanemab exposure (AUC), a separate analysis was conducted to evaluate the potential clinical importance of exposure differences on efficacy and safety in subjects with low (51 kg, 5th percentile) and high (99 kg, 95th percentile) body weights. The effect of body weight on efficacy as measured by reduction in brain amyloid load was evaluated by simulation analyses using PK/PD model for PET SUVr. The simulation results demonstrated comparable reduction in SUVr following a 720 mg SC weekly dose and 10 mg/kg biweekly IV dose for a typical 70 kg subject. Small differences in the reduction in PET SUVr for a subject with high (95th percentile) or low (5th percentile) body weight as demonstrated by simulation analysis are not considered to be clinically important. Thus, lecanemab exposure differences observed at the extremes of body weight are not expected to have a meaningful effect on lecanemab efficacy as defined by PET SUVr. The effect of body weight on lecanemab safety defined as incidence of ARIA-E was also evaluated by simulation analysis based on PK/PD model. Based on initial analysis of a PK/PD model for ARIA-E developed using data from Study 201, lecanemab maximum serum concentration (Cmax) was a significant predictor of the risk of ARIA-E. Based on the results of Study 004, following single doses, subcutaneous administration of lecanemab resulted in approximately 4-fold lower Cmax compared to intravenous. Thus, the incidence of ARIA-E following subcutaneous administration was expected to be substantially lower compared to intravenous administration. According to the model-based simulation analysis, the incidence of ARIA-E in the first 6 months of treatment is predicted to be 2.1% (1.2%) for 720 mg weekly SC dose compared to 9% (3.7%) for 10 mg/kg biweekly IV dose for APOE4 carrier (APOE4 Attorney Docket No.08061.0062-00304 noncarrier) subjects. Data from the Phase 3 Study indicate that the incidence of ARIA-E with SC administration was similar to the incidence of ARIA-E with IV administration. The incidence of ARIA-E was related to the AUC (and average plasma concentration (Cave)), rather than Cmax. ARIA-E incidence in subjects with high (95th percentile) or low (5th percentile) body weight was comparable to that in a subject with a reference 70 kg body weight as demonstrated by simulation analysis. The probability of experiencing ARIA-E following subcutaneous weekly administration is predicted to be lower than following intravenous biweekly and minimally affected by body weight. In summary, exposure-response simulations using PET SUVr as a measure of efficacy and incidence of ARIA-E as a measure of safety demonstrated no clinically important effect of body weight, confirming that the proposed fixed subcutaneous dose can be administered to all subjects without regard for body weight. The 720 mg weekly SC AI dose will be optimized to 500 mg weekly. The 500 mg weekly SC AI dose was selected based upon an analysis of all PK data collected to date using the SC route of administration. The results of Study 005 demonstrated that exposure following AI administration was approximately 20% greater than following administration with the reference vial and syringe method (Geometric Mean AUC_0-inf 20900 µg.h/mL [AI] and 17500 µg.h/mL [vial and syringe], Study 005 CSR Table 16). The greater exposure with AI administration relative to vial/syringe was confirmed in an analysis of Study 301 Extension Phase data. The assessment Study 301 Extension Phase SC Substudies data also revealed that bioavailability following SC administration is higher in AD patients than had been predicted in Study 004, a healthy volunteer study comparing IV administration with vial/syringe administration. A comparison of average steady-state lecanemab concentrations from subjects administered 10 mg/kg biweekly lecanemab in Study 301 Core or OLE and those administered 720 mg SC AI weekly is provided in Figure 39 (AI = autoinjector, OLE = open-label extension, IV = intravenous). Together, these results were used to project that a dose of 500 mg weekly using the AI would yield average steady-state lecanemab concentrations similar to those produced by a dose of 10 mg/kg biweekly administered via the IV route (Error! Reference source not found.). In Figure 40, model predicted/observed IV LEC10-BW data from Study 301 Core/OLE (n=1504), projected 500 mg QW SC AI values based on model predicted average steady-state concentration following 720 mg QW AI (n=256). AI = autoinjector, C_ave,ss = average steady-state concentration, IV = intravenous, LEC10-BW = lecanemab 10 mg/kg biweekly, QW = once weekly, SC = subcutaneous. By producing similar steady-state lecanemab concentrations, exposure-response models developed for amyloid PET and change in disease progression (measured by CDR-SB) predict that 500 mg weekly AI will have similar efficacy as the 10 mg/kg biweekly IV dosing regimen (Error! Reference source not found. and Error! Reference source not found.). In Figure 41, amyloid PET Attorney Docket No.08061.0062-00304 simulations were conducted using a PK model developed using all PK data following either IV or SC administration that was available as of 30 Nov 2023, and the amyloid PET PK/PD model. Each scenario represents 7000 simulated subjects, with demographics sampled with replacement from the combined Study 201 Core and Study 301 Core subject populations. Solid lines represent median projected amyloid PET, shaded regions represent 90% prediction interval. AI = autoinjector, BW = biweekly; IV = intravenous, PET = positron emission tomography, QW = once weekly, SC = subcutaneous. In Figure 42, simulations were conducted using a PK model developed using all PK data following either IV or SC administration that was available as of 30 Nov 2023, and the amyloid PET PK/PD and amyloid PET-CDR-SB models. Each scenario represents 7000 simulated subjects, with demographics sampled with replacement from the combined Study 201 Core and Study 301 Core subject populations. Solid lines represent average projected change in CDR-SB, shaded regions represent 90% prediction interval. AI = autoinjector, BW = biweekly, CDR-SB = Clinical Dementia Rating-Sum of Boxes, IV = intravenous, QW = once weekly, SC = subcutaneous. Preliminary PK data from the subcutaneous AI substudy in subjects receiving 720 mg SC is composed of 2 consecutive (ie, “back-to-back”) injections of 360 mg (2x1.8mL of 200 mg/mL SC formulation), together with PK/PD analyses, demonstrated that after initial 18 to 24 months of treatment with 10 mg/kg IV biweekly and/or 720 mg SC weekly, subjects can be transitioned to a lower maintenance dose of 360 mg SC weekly. This maintenance dose of 360 mg SC weekly is expected to further reduce brain amyloid in all subjects and sustain continued clinical benefit for all subjects, regardless of whether they achieved amyloid negativity (defined as amyloid PET <30 Centiloid) at 18 months (Error! Reference source not found. and Figure 44). Figure 43 shows the projected change in amyloid PET for subjects receiving 10 mg/kg IV for 18 or 24 months, followed by 360 mg SC AI weekly compared to placebo or continuous 10 mg/kg IV lecanemab. Figure 44 shows the projected change in CDR-SB for subjects receiving 10 mg/kg IV for 18 or 24 months, followed by 360 mg SC AI weekly compared to placebo or continuous 10 mg/kg IV lecanemab. Amyloid PET simulations conducted using a PK model developed using all PK data following either IV or SC administration that was available as of 30 Nov 2023, and the amyloid PET PK/PD model. Each scenario used post hoc model parameters from all subjects with amyloid imaging in Study 301 to project amyloid PET over time, with subjects receiving either continuous LEC10-BW for 48 months, or transitioning to 360 mg SC AI Weekly at 18 or 24 months. Solid lines represent average projected change in amyloid PET. AI = autoinjector, BW = biweekly, IV=intraveneous, LEC10-BW = 10 mg/kg IV lecanemab biweekly, PET = positron emission tomography, SC = subcutaneous. Attorney Docket No.08061.0062-00304 CDR-SB simulations conducted using a PK model developed using all PK data following either IV or SC administration that was available as of 30 Nov 2023, as well as the amyloid PET PK/PD and amyloid PET-CDR-SB models. Each scenario used post hoc model parameters from all subjects with amyloid imaging in Study 301 to project mean change in CDR-SB over time, with subject receiving either continuous LEC10-BW for 48 months, or transitioning to 360 mg SC AI Weekly at 18 or 24 months. AI = autoinjector, CDR-SB = Clinical Dementia Rating-Sum of Boxes, IV = intravenous, LEC10-BW = lecanemab 10 mg/kg IV biweekly, SC = subcutaneous. Applying the same methodology as was used for IV maintenance, PK/PD simulations for SC maintenance dosing were conducted to estimate the change in amyloid PET and CDR-SB under the scenarios where the patients were assigned to placebo, continuous IV LEC10-BW, or where SC or IV maintenance dosing was initiated at 18 and 24 months. These simulations incorporate a PK model developed based on data from the Study 301 OLE AI substudy to simulate exposures following 360 mg QW AI administration. Data from Study 301 Core and OLE demonstrated that subjects with lower amyloid baseline (<60 Centiloids) progress more slowly compared to subjects with amyloid baseline (>60 Centiloids) suggesting that amyloid PET baseline affects clinical disease progression. Considering these differences in disease progression for subjects with different amyloid baseline, simulation analyses were conducted in populations with baseline amyloid PET above and below 60 Centiloids. These simulations demonstrate that initiation of the SC 360 mg QW maintenance dose (1x AI Device) after 18 and 24 months of IV LEC10-BW results in similar amyloid removal and clinical efficacy as compared to continued IV LEC10-BW for 4 years or switching to IV LEC10-M maintenance dose at 18 and 24 months (Figure 45 and Figure 46). Predicted biomarker changes (Figure 47) further support Eisai’s proposal for the weekly SC AI Device maintenance dosing regimen as it would maintain plasma biomarkers at levels consistent with lecanemab efficacy. Overall, initiation of the SC 360 mg QW (1x AI Device) maintenance dose will sustain the benefit of lecanemab treatment and would provide the additional patient convenience of at home administration. Figure 45 shows simulated amyloid PET profiles for IV LEC10-BW dosing for 4 years, compared to initiation of SC 360 mg QW (1x AI Device) or LEC10-M, for a maintenance dose at 18 and 24 months in subjects with baseline amyloid PET ≥60 and <60 Centiloids. AI = autoinjector, BW = biweekly, CL = Centiloids, IV = intravenous, PET = positron emission tomography, QW = weekly, Q4W = every 4 weeks. Figure 46 shows simulated CDR-SB profiles for IV LEC10-BW Dosing for 4 Years, compared to initiation of SC 360 mg QW (1x AI Device) or LEC10-M, for a maintenance dose at 18 and 24 months in subjects with baseline amyloid PET ≥60 and <60 Centiloids. AI = autoinjector, BW Attorney Docket No.08061.0062-00304 = biweekly, CL = Centiloids, IV = intravenous, PET = positron emission tomography, QW = weekly, Q4W = every 4 weeks. Figure 47 shows model-predicted plasma Aβ42/40 ratio and p-tau181 after various dosing regimens. AI = autoinjector, BW = biweekly, CI = Confidence Intervals, QW = weekly, Q4W = every 4 weeks. Solid line and shaded area show predicted median and 95% CI, respectively. P-tau181 = human tau protein phosphorylated at threonine in position 181. Figure 48 shows SC exposures in healthy volunteers (Study 005) and Study 301 OLE AI device substudy (AD subjects) compared to IV LEC10-BW. AD = Alzheimer’s disease; HV = healthy volunteers; IV = intravenous; n=168 with both IV and AD device. The PK data from the Study 301 OLE SC AI Device substudy in subjects receiving SC 720 mg QW (2x AI Devices) have been utilized to estimate individual Cave,ss for SC 360 mg QW (1x AI Device) using a population PK model. Figure 49 shows SC exposures following 360 mg QW AI maintenance doses are within the range of LEC10-BW. Mean model predicted lecanemab exposure following a SC 360 mg QW (1x AI Device) maintenance dose is 25% lower than IV LEC10-BW and below the range observed for IV LEC10-BW. Thus, the safety database defined in studies with IV lecanemab fully support the SC 360 mg QW (1x AI Device) maintenance dose in subjects with EAD. 13. Preliminary Data from the Study 301 OLE Subcutaneous Substudies a. Preliminary Data from the SC Vial Substudy Preliminary PK data from the subcutaneous AI substudy in subjects receiving 720 mg SC is composed of 2 consecutive (ie, “back-to-back”) injections of 360 mg (2x1.8mL of 400 mg/2 mL SC formulation), together with PK/PD analyses, demonstrated that after initial 18 to 24 months of treatment with 10 mg/kg IV biweekly and/or 720 mg SC weekly, subjects can be transitioned to a lower maintenance dose of 360 mg SC weekly. This maintenance dose of 360 mg SC weekly is expected to further reduce brain amyloid in all subjects and sustain continued clinical benefit for all subjects. Table 18 shows the preliminary results of a PD comparability analysis in lecanemab-naïve subjects who were enrolled in the SC Vial substudy.70 out of 72 of these subjects have completed both 6 months of treatment at 720 mg QW and the 6-month amyloid PET scan.63 subjects completed 12 months of treatment. Preliminary results of a PD comparability analysis using an analysis of covariance (ANCOVA) model which included baseline amyloid PET (Centiloids), age, and treatment showed that SC administration via vial and syringe resulted in 15% greater amyloid removal compared to IV administration. The 90% confidence interval (CI) for the ratio of change from Attorney Docket No.08061.0062-00304 baseline (CFB) SC to IV was 103-127%. The impact of body weight, APOE4 genotype, and disease status was also evaluated in this ANCOVA model. Body weight, APOE4 genotype, and disease status are not statistically significant covariates in this model. The sample size is too small to perform subgroup analysis, however the ratio is close to 100% in each of these subgroups. Therefore, the Study 301 OLE SC Vial substudy validates the PD comparability of an SC formulation to the IV formulation. Table 18. Preliminary results for PD comparability of lecanemab SC and IV administration at 6 months and 12 months (amyloid PET centiloids) CFB in Amyloid PET Results of PD Comparability Analysis IV SC R ti LB f 90% UB f )

V = intravenous, SC = subcutaneous, SE = standard error, UB = upper bound. Source: ANCOVA model with covariates = treatment, baseline centiloids, age. Table 19 shows PK comparability for IV and SC vial administration was also established based on bioequivalence (BE) analysis in PK data available from 65 subjects in the SC Vial substudy receiving both IV and SC vial. Table 19. Bioequivalence evaluation of lecanemab following administration via SC Vial (Test) and IV (Reference)

Table 19 shows PK comparability for IV and SC vial administration was also established based on bioequivalence (BE) analysis in PK data available from 65 subjects in the SC Vial substudy receiving both IV and SC vial. Attorney Docket No.08061.0062-00304 b. Preliminary Data from the SC AI Device Substudy In the Study 301 OLE SC AI Device substudy, 257 subjects received weekly doses of 720 mg (2 consecutive SC injections of 360 mg) using AI Devices after at least 6 months of IV LEC10- BW treatment. The population PK model predicted average steady-state concentrations (Cave,ss) of lecanemab following the 720 mg QW SC AI Device administration in these subjects was ~30% higher compared to IV LEC10-BW and is above Cave,ss in healthy subjects predicted based on the Study 005 results (Figure 49). Based upon these results, a lower optimized dose for the SC AI Device is needed to achieve exposures comparable to LEC10-BW. Figure 49 shows SC exposures in Study 005 (healthy volunteers) and Study 301 OLE AI device substudy (AD subjects) compared to IV LEC10- BW. AD = Alzheimer’s disease; HV = healthy volunteers; IV = intravenous; n=168 with both IV and AD device. c. Preliminary Safety Data Preliminary safety data is available for 394 subjects (data cutoff 22 Sep 2023, 6 months) in the SC Vial/AI Device substudies (which includes the 72 SC lecanemab-naïve subjects). Rates of ARIA-E and ARIA-H are provided in Table 20 for ‘All Phase 3 SC’ subjects and lecanemab naïve subjects (‘SC LEC-Naïve’). As with IV administration, ARIA-E occurs early in treatment and was mostly asymptomatic and radiographically mild to moderate in severity. ARIA-H is randomly distributed throughout the treatment period and was almost always asymptomatic. The rates of systemic injection reactions are lower with SC administration (SC lecanemab- naïve: 0/72 [0%] subjects; All Phase 3 SC: 2/394 [0.5%] subjects, both mild in severity) compared to IV (236/898 [26.3%] subjects. We believe SC lecanemab-naïve subjects are the appropriate comparison with IV administration as systemic reactions occur early in treatment with lecanemab. There was also a low rate of local injection site reactions, with most mild and moderate in severity (reported symptoms: redness, irritation, and swelling). There were no skin rash or other hypersensitivity reactions reported. The available results from the SC substudies support an improved safety profile with regard to systemic injection/infusion related reactions. Table 20. Safety in subjects receiving lecanemab SC administration (SC Vial or AI Device) in Study 301 OLE Phase Attorney Docket No.08061.0062-00304

After 12 months (data cutoff March 31, 2024, 12 months) in the SC Vial/AI Device substudies, the incidence of ARIA-E and ARIA-H are similar to the 6 month data in the 394 subjects (Table 21). Table 21. Safety in subjects receiving lecanemab SC administration (SC Vial or AI Device) in Study 301 OLE Phase at 6 months and 12 months (A) 6 months (ARIA-E data) Lecanemab SC (vial Lecanemab SC LEC-

Attorney Docket No.08061.0062-00304 ApoE4 heterozygote 3/214 (1.4%) 3/39(7.7%) ApoE4 homozygote 1/47 (2.1%) 0/6

Lecanemab SC (vial or AI) Lecanemab SC LEC-Naive

(C) 12 months (ARIA-E and ARIA-H data) Lecanemab SC Lecanemab SC (vial or AI) LEC-Naive

Attorney Docket No.08061.0062-00304 Macrohemorrhage 1 (0.25) 0 Isolated ARIA-H 40 (102) 8 (111)

. Stat st ca na yses a. Analysis Sets The Extension Full Analysis Set (Extension-FAS) is the group of subjects who received at least 1 dose of study drug during the Core Study and who had a baseline assessment and at least 1 postdose primary efficacy measurement during the Extension Phase. The Extension Safety Analysis Set is the group of subjects who received at least 1 dose of study drug during the Extension Phase The Extension PK Analysis Set is the group of subjects who received at least 1 dose of study drug during the Core Study with at least 1 quantifiable BAN2401 serum (analysis set for serum) or CSF concentration (analysis set for CSF) with a documented dosing history during the Extension Phase. The Extension PD Analysis Set is the group of subjects who received at least 1 dose of study drug during the Core Study and had sufficient PD data to derive at least 1 PD parameter (have baseline and at least 1 postdose assessment) during the Extension Phase. b. Subcutaneous Substudies Analysis Sets The Safety Analysis Set is the group of subjects who received at least 1 of the 2 injections required for the 720 mg dose (i.e., 2 injections of 360 mg) of study drug administered subcutaneously using SC vial or the AI Device over the Extension Phase subcutaneous treatment period. The Safety Analysis Set will be used for safety analyses of the subcutaneous vial and AI substudies. The analysis period for safety analyses includes the subcutaneous treatment period during the Extension Phase, which will be described as “SC-treated period”. Subcutaneous baseline (i.e., baseline of the subcutaneous vial or AI substudies) is the last nonmissing assessment before the start of the 1st lecanemab subcutaneous (vial or AI) treatment. To assess change from baseline, a baseline measurement is also required. The safety data will be presented in 1 group which includes all subjects in the Safety Analysis Set. Some safety analyses will also be provided for lecanemab-naïve subjects (de novo subjects plus newly-treated Core placebo subjects) in the Safety Analysis Set. The analysis period for these safety analyses includes the subcutaneous vial treatment period during the Extension Phase, which will be described as “SC vial treated period”. Attorney Docket No.08061.0062-00304 The PD Analysis Set for amyloid PET using Centiloids is the group of subjects who received at least 1 full dose (i.e., 2 injections of 360 mg) of study drug administered subcutaneously using SC vial or the AI Device over the subcutaneous treatment period and had amyloid PET using Centiloids assessment at subcutaneous baseline and at least 1 postbaseline amyloid PET using assessment during that period. Similar definition applies to the PD Analysis Set for biomarkers such as amyloid PET by visual read, plasma Aβ42/40, plasma p-tau 181, GFAP, and NfL. The PK Analysis Set is the group of subjects who received at least 1 full dose (i.e., 2 injections of 360 mg) of study drug administered subcutaneously using SC vial or the AI Device over the subcutaneous treatment period and with at least 1 quantifiable BAN2401 serum concentration (analysis set for serum) or CSF concentration (analysis set for CSF) during that period. c. Subcutaneous 360 mg AI Substudy Analysis Sets The Safety Analysis Set is the group of subjects who received at least one 360 mg dose injection of study drug administered subcutaneously using the AI over the Extension Phase subcutaneous 360 mg AI treatment period. The Safety Analysis Set will be used for safety analyses of the subcutaneous 360 mg AI dose substudy. The analysis period for safety analyses includes the dose treatment period during the Extension Phase, which will be described as “SC-360 mg AI dose period”. Subcutaneous 360 mg AI dose baseline is the last nonmissing assessment before the start of the 1st subcutaneous 360 mg AI dose. To assess change from baseline, a baseline measurement is also required. The safety data will be presented in 1 group which includes all subjects in the Safety Analysis Set. The PD Analysis Set for plasma Aβ42/40 is the group of subjects who received at least one 360 mg AI dose injection of study drug administered subcutaneously using the AI over the subcutaneous 360 mg AI treatment period and had plasma Aβ42/40 assessment at subcutaneous 360 mg AI dose baseline and at least one postbaseline plasma Aβ42/40 assessment during that period. Similar definition applies to the PD Analysis Set for other plasma biomarkers. The PK Analysis Set is the group of subjects who received at least one 360 mg AI dose injection of of study drug administered subcutaneously using the AI over the subcutaneous 360 mg AI treatment period and with at least one quantifiable BAN2401 serum concentration (analysis set for serum) or CSF concentration (analysis set for CSF) during that period. 15. Study Endpoints a. Primary Endpoints Incidence of AEs and changes in vital signs, ECGs, laboratory safety tests, suicidality assessments, ADAs, and MRI safety parameters. Change from Core Study baseline in CDR-SB. Attorney Docket No.08061.0062-00304 b. Exploratory Endpoints Change from Core Study baseline in: ADAS-Cog14, ADCOMS, ADCS MCI-ADL, and modified iADRS Brain amyloid and tau PET levels Blood and CSF biomarkers (neurogranin [CSF only], NFL, Aβ[1-42], Aβ[140], plasma Aβ42/40 ratio, t-tau, and p-tau [including, but not limited to p-tau181]) vMRI biomarkers EQ-5D-5L, QOL-AD, and Zarit Burden Interview Proportion of subjects who convert from amyloid positive to amyloid negative by visual read, SUVR, and Centiloids Correlation between clinical changes (CDR-SB, ADAS-Cog14, ADCOMS, ADCS MCI- ADL, and modified iADRS) and changes in biomarkers of AD pathology (including but not limited to, amyloid PET, tau PET, blood and CSF biomarkers [Aβ[1-42], Aβ[1-40], plasma Aβ42/40 ratio, neurogranin, NFL, t tau, and p tau [including, but not limited to p-tau181]) Describe the characteristics, comorbidities, treatments, associated costs for subjects with EAD, and study partner burden at baseline, before study enrollment, during study participation (including Core Study and Extension Phase), and after study completion 16. Subcutaneous Substudies Endpoints a. Primary Endpoints: Incidence of AEs and changes in vital signs, ECGs, laboratory safety tests, suicidality assessments, ADAs, and MRI safety parameters when BAN2401 is administered subcutaneously Population PK parameters of BAN2401 in serum, including but not limited, to AUC, Cav. b. Secondary Endpoints: Incidence and timing of ADA onset, ADA titer, and other characteristics related to subject ADA status over the subcutaneous treatment period, and incidence and timing of NAb onset, NAb titer, and other characteristics related to subject NAb status over the subcutaneous treatment period Change from baseline in brain amyloid levels over the subcutaneous treatment period Proportion of subcutaneous substudy subjects who convert from amyloid positive to amyloid negative by visual read, SUVR, and Centiloids over the subcutaneous treatment period Change from subcutaneous substudies baseline in plasma biomarkers (i.e., p-tau181) over the subcutaneous treatment period. Attorney Docket No.08061.0062-00304 c. Exploratory Endpoint: Compliance of subcutaneous administration of BAN2401 using an AI device. 17. Subcutaneous 360 mg AI Dosing Endpoints a. Primary Endpoints: Incidence of AEs and changes in vital signs, ECGs, laboratory safety tests, suicidality assessments, ADAs, and MRI safety parameters when BAN2401 is administered subcutaneously following a subcutaneous 360 mg AI dosing regimen. Incidence and timing of ADA onset, ADA titer, and other characteristics related to subject ADA status over the subcutaneous 360 mg AI treatment period, and incidence and timing of NAb onset, NAb titer, and other characteristics related to subject NAb status over the subcutaneous treatment period when BAN2401 is administered following a subcutaneous 360 mg AI dosing regimen. b. Secondary Endpoints: Population PK parameters of BAN2401 in serum when BAN2401 is administered following a subcutaneous 360 mg AI dosing regimen, including but not limited, to AUC, Cav. 18. Analyses a. Statistical Methods The following analyses describe the statistical methods for the analysis of data from Baseline through Extension Phase. b. Biomarker and Clinical Efficacy Analyses An MMRM will be used to analyze change from Core Study baseline in the following: Clinical endpoints: CDR-SB, ADAS-Cog14, ADCOMS, ADCS MCI-ADL, modified iADRS, and MMSE EQ-5D-5L, QOL-AD, and Zarit Burden Interview Biomarkers: amyloid PET using Centiloids, amyloid PET SUVR composite, tau PET SUVR, in whole cortical gray matter ROI, meta-temporal ROI, frontal ROI, cingulate ROI, parietal ROI, occipital ROI, medial temporal ROI, and temporal ROI and TauIQ global tau load, blood and CSF biomarkers (Aβ[1-42], Aβ[1-40], plasma Aβ42/Aβ40 ratio, neurogranin (CSF only), NFL, t-tau and p-tau [including, but not limited to p-tau181]), and vMRI Additional analyses and summaries will be performed as appropriate. Attorney Docket No.08061.0062-00304 c. Safety Analyses Similar analyses with Core Study will be conducted. d. Subcutaneous (vial, AI, AI subcutaneous 360 mg AI dosing) Substudies Analyses Statistical analyses for the subcutaneous vial, the subcutaneous AI substudies, and the subcutaneous 360 mg AI substudies will be conducted. Example 7: Subcutaneous Administration of 500 mg of Lecanemab In a further study, a 500 mg SC AI dose will be administered weekly. The 500 mg weekly SC AI dose was selected based upon an analysis of all PK data collected to date using the subcutaneous route of administration. The results of Study 005 demonstrated that exposure following AI administration was approximately 20% greater than following administration with the reference vial and syringe method. The greater exposure with AI administration relative to vial/syringe was confirmed in an analysis of Study 301 OLE data. The assessment of data in Study 301 OLE also revealed that bioavailability following SC administration is higher in AD patients than had been predicted in Study 004, a healthy volunteer study comparing IV administration with vial/syringe administration. Together, these results were used to project that a dose of 500 mg weekly using the AI would yield average steady-state lecanemab concentrations similar to those produced by a dose of 10 mg/kg biweekly administered via the IV route. By producing similar steady-state lecanemab concentrations, exposure-response models developed for amyloid PET and change in disease progression (measured by CDR-SB) predict that 500 mg weekly AI will have similar efficacy as the 10 mg/kg biweekly IV dosing regimen. The 500 mg weekly AI dose may be administered subcutaneously to subjects who were on any prior regimen (e.g., 10 mg/kg IV biweekly, 720 mg SC vial, or 720 SC AI). PK data will be collected for the 500 mg weekly dose. The 500 mg dose will be administered by AI. Example 8: Maintenance dosing Results from further studies and/or modeling will show effects of different maintenance doses: 360 mg or 250 mg SC AI administered weekly or 10 mg/kg IV administered monthly. The maintenance doses (either 10 mg/kg IV monthly or 360 mg SC weekly or 250 mg SC weekly) are intended to follow 18 months of initiation doses (either 10 mg/kg IV biweekly or 720 mg SC weekly or 500 mg SC weekly). Any permutation of initiation dose with maintenance dose is allowed. All SC doses will be administered by autoinjector (e.g., 360 mg SC AI or 250 mg SC AI). Attorney Docket No.08061.0062-00304 1. Intravenous Maintenance Dosing Regimen The maintenance dose of BAN2401 (LEQEMBI) will be 10 mg/kg iv once every 4 weeks (i.e., monthly). LEQEMBI may be diluted then administered and then administered as an intravenous infusion over approximately one hour. This IV maintenance dose is selected based on modeling of observed data from Study 201 and the open-label (OLE) Clarity AD study (Study 301), both summarized above. In studies of IV doses, steady-state concentrations of lecanemab-irmb were reached after 6 weeks of iv administration at 10 mg/kg administered every 2 weeks, and systemic accumulation was 1.4-fold. The peak concentration (Cmax) and area under the plasma concentration versus time curve (AUC) of lecanemab-irmb increased dose proportionally in the dose range of 0.3 to 15 mg/kg following single dose. In patients receiving 10 mg/kg once every 2 weeks, average (± standard deviation) steady state concentration is estimated to be 148 (±50) mcg/mL. In patients receiving 10 mg/kg once every 4 weeks, average (± standard deviation) steady-state concentration is estimated to be 71.2 (±20) mcg/mL. Thus, an intravenous initiation dosing regimen may comprise a dosage of BAN2401 (LEQEMBI) that is 10 mg/kg administered once every 2 weeks (i.e., biweekly), for a period of time, e.g., 18 months or 24 months, after which the initiation dosing regimen is switched to a maintenance dosing regimen comprising a dosage of BAN2401 (LEQEMBI) that is 10 mg/kg administered once every 4 weeks (i.e., monthly) which, without being bound by theory, may maintain steady state lecanemab-irmb concentration and/or continue to stabilize or further reduce amyloid protofibril in subjects. Example 9: Neuro-Dynamic Quantitative Systems Pharmacology (QSP) Model Supports Continued Lecanemab Treatment with Maintenance Dosing for Alzheimer’s Disease QSP modeling and simulations may integratively explain multivariate data based on AD pathophysiology and provide insights and rationales to support continued lecanemab treatment with proposed maintenance dosing. Background: Lecanemab, an approved humanized IgG1 monoclonal antibody that binds with high affinity to Aβ protofibrils, demonstrated significant clinical benefit in slowing cognitive decline in early Alzheimer’s disease (AD) in two clinical studies (NCT01767311 and CLARITY-AD, NCT03887455). A less frequent maintenance dosing (MD) is proposed after a sufficient initial biweekly (LEC10-BW) treatment. To further understand long-term benefit of continued lecanemab treatment with MD, a quantitative systems pharmacology (QSP) model was developed to mechanistically describe AD pathophysiology using multivariate data from clinical studies. Attorney Docket No.08061.0062-00304 Methods: The model incorporated three interlinked modules describing Aβ pathway, tau pathology and cognitive decline, where Aβ triggers tau pathology and tau pathology leads to cognitive decline due to neuronal damage and degeneration. The population QSP model was developed in Monolix using nonlinear mixed-effect modeling. The model was adequately informed and successfully validated using a multivariate dataset (N=4057) consisting of amyloid PET, CDR-SB, ADAS-Cog, plasma Aβ42/40 ratio and pTau181, and Tau PET from lecanemab Phase 2 and 3 trials, as well as amyloid PET, ADAS-Cog and CDR-SB data from the Alzheimer’s Disease Neuroimaging Initiative (ADNI). QSP model-based simulations were conducted to investigate long-term lecanemab benefits with different dosing frequencies of MD following the initial LEC10-BW treatment. Results: QSP simulations showed additional benefits can be gained across clinical outcomes, amyloid plaque and protofibrils, Tau PET, and plasma biomarkers with continued lecanemab treatment beyond 18-month. Specifically, lecanemab monthly MD (LEC10-M) following the initial treatment continues to reduce brain amyloid plaques and protofibrils in subjects who did not reach amyloid negativity with 18-month LEC10-BW. Simulations showed plasma pTau-181 continue to decline and plasma Aβ42/40 ratio continue to increase with LEC10-M MD. Furthermore, simulations showed tau PET accumulation continued to be suppressed with LEC10-M MD, and consequently led to additional reductions in cognitive decline (CDR-SB, ADAS-Cog). Simulations indicated that sustained protofibril clearance is a key driver for long-term (>18 months) lecanemab effect on halting tau pathology and slowing cognitive decline, particularly after plaques are cleared following lecanemab treatment. Example 10: Model-Based Assessment of Lecanemab Maintenance Dosing Regimen Shows Continued Suppression of Amyloid Plaque, Disease Progression Models of lecanemab dosing provide insight for transitioning patients to maintenance dosing. Background: Lecanemab is a humanized IgG1 monoclonal antibody that binds with high affinity to Aβ soluble protofibrils. Lecanemab has been tested as a disease-modifying treatment for early Alzheimer’s disease in two clinical studies (NCT01767311 and CLARITY-AD, NCT03887455). Amyloid PET and CDR-SB were assessed throughout the trials, and these data were used to develop models describing the change in these endpoints in response to lecanemab treatment. These models were used to explore the impact of changing from the initial dosage regimen (10 mg/kg Q2W) to a less intensive dosing regimen (10 mg/kg Q4W) on clinical efficacy, and to explore the optimal duration of the initial dosing regimen. Methods: Models describing the relationship between serum lecanemab exposure, amyloid PET, and CDR-SB have been previously described. Individual post hoc model estimates for PK, PET, Attorney Docket No.08061.0062-00304 and CDR parameters were obtained from Study 301 subjects who received lecanemab and were used to simulate change in amyloid PET and CDR-SB over 4 years. Simulations were conducted to evaluate the effect of lecanemab (10 mg/kg IV Q2W) after continuous treatment or transitioning to a less intensive dosing regimen (10 mg/kg Q4W) at 18 or 24 months. Simulations were conducted for subjects with baseline amyloid PET <60 CL and ≥60 CL. Results: After 18 months of treatment, the mean amyloid PET level was ≤25 CL in both the high and low baseline PET groups. Regardless of whether patients transitioned to a Q4W regimen, continued treatment resulted in modest (≤15 CL) additional reduction of amyloid PET over 4 years of treatment. The difference in amyloid reduction between continuous Q2W treatment and Q4W treatment initiated at 18 months was 2.5 CL in the low baseline PET group and 5.1 CL in the high baseline PET group. No significant difference in CDR-SB was projected between subjects receiving Q2W lecanemab for 4 years, or transitioning to Q4W dosing, regardless of when the subjects transitioned. Conclusions: Subjects receiving lecanemab 10 mg/kg Q2W may transition to a less intensive (Q4W) maintenance regimen after 18 months. The maintenance regimen has no clinically meaningful impact on amyloid or disease progression relative to the Q2W regimen. Example 11: Lecanemab Stabilizes Tau PET Effects of lecanemab treatment on tau accumulation may be determined by tau PET imaging. Quantitative systems pharmacology (QSP) modeling enables integrated assessment of the effect of lecanemab treatment on tau pathology. Background: Lecanemab is an approved anti-amyloid monoclonal antibody that binds with highest affinity to soluble Aβ protofibrils, which are more toxic than monomers or insoluble fibrils/plaque. In clinical studies, lecanemab demonstrated a slowing of decline in clinical (global, cognitive, functional, and quality of life) outcomes, and reduction in brain amyloid in early Alzheimer’s disease (AD). Herein, we describe the impact of lecanemab treatment on tau PET. Methods: Changes over time in tau PET SUVR ([18F]MK6240) were compared between placebo and lecanemab-treated groups. Associations between baseline and change from baseline (CFB) in tau PET SUVR across brain regions were investigated. A quantitative systems pharmacology (QSP)model was developed to describe the dynamics of medial temporal (MTL) tau PET based on AD pathophysiology with three interlinked modules: Aβ pathway, tau pathway, and cognitive function. MTL tau PET data from Clarity AD and other biomarkers from Clarity AD and Study 201, and Alzheimer's Disease Neuroimaging Initiative (ADNI), were used to inform and validate the model. QSP model-based simulations were conducted to investigate the effect of lecanemab treatment on tau pathology. Attorney Docket No.08061.0062-00304 Results: Higher baseline tau levels were associated with higher tau accumulation across brain regions with disease progression. Lecanemab treatment significantly slowed accumulation of tau in temporal regions relative to placebo and disrupted association between baseline tau and CFB in tau across brain regions. QSP simulations predicted MTL tau PET accumulates 0.064 SUVR points per year (ppy) in placebo, and 0.092 ppy in high baseline tau group (tau PET SUVR>1.5). QSP simulations predicted that lecanemab treatment halted tau PET accumulation in MTL region within 18 months of treatment and maintained suppression with continued biweekly lecanemab regardless of baseline tau levels. Conclusions: Lecanemab treatment demonstrated an impact on tau accumulation across brain regions. The QSP model adequately described MTL tau PET for placebo and lecanemab across 30 months of Clarity AD data. QSP simulations suggest that lecanemab halts tau PET accumulation by clearing major tau pathology drivers of amyloid protofibril and plaque, slowing down long-term cognitive decline. Taken together, tau PET data and QSP modeling support additional benefits of continued lecanemab treatment. EQUIVALENTS AND SCOPE Those skilled in the art will recognize that where ranges are given, endpoints are included. Furthermore, it is to be understood that unless otherwise indicated or otherwise evident from the context and understanding of one of ordinary skill in the art, values that are expressed as ranges can assume any specific value or subrange within the stated ranges in different embodiments of the disclosure. In addition, it is to be understood that any particular embodiment of the present disclosure that falls within the prior art may be explicitly excluded from any one or more of the claims. Since such embodiments are deemed to be known to one of ordinary skill in the art, they may be excluded even if the exclusion is not set forth explicitly herein. Any particular embodiment of the compositions of the disclosure (e.g., any, composition, therapeutic or active ingredient; any method of production; any method of use; etc.) can be excluded from any one or more claims, for any reason, whether or not related to the existence of prior art. It is to be understood that the words which have been used are words of description rather than limitation, and that changes may be made within the purview of the appended claims without departing from the true scope and spirit of the disclosure in its broader aspects. While the present disclosure has been described at some length and with some particularity with respect to the several described embodiments, it is not intended that it should be limited to any such particulars or embodiments or any particular embodiment, but it is to be construed with references to the appended claims so as to provide the broadest possible interpretation of such Attorney Docket No.08061.0062-00304 claims in view of the prior art and, therefore, to effectively encompass the intended scope of the disclosure. All publications, patent applications, patents, and other references mentioned herein are incorporated by reference in their entirety. In case of conflict, the present specification, including definitions, will control. In addition, section headings, the materials, methods, and examples are illustrative only and not intended to be limiting.

Claims

Attorney Docket No.08061.0062-00304 CLAIMS 1. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising subcutaneously administering to the subject 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg), of an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3). 2. A method of delaying clinical decline in a subject having AD, suspected of having AD, or at risk for AD, comprising subcutaneously administering to the subject 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg), of an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences 3. A method of reducing brain amyloid level in a subject having AD, suspected of having AD, or at risk for AD, comprising subcutaneously administering to the subject 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg), of an antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3). 4. A method of converting an amyloid positive subject to amyloid negative, comprising subcutaneously administering to the subject 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg), of an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3). 5. The method of any one of claims 1-4, wherein the anti-Aβ protofibril antibody is subcutaneously administered at 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg) reduces a biomarker of AD pathology and/or provides a lower systemic exposure (e.g., AUC) to the antibody than for a higher dose such as 720 mg administered subcutaneously. Attorney Docket No.08061.0062-00304 6. The method of any one of claims 1-5, wherein the anti-Aβ protofibril antibody is subcutaneously administered at 150 mg to 600 mg, e.g., 200 mg to 550 mg (e.g., 500 mg) reduces a risk for developing ARIA relative to a higher dose of the antibody, such as 720 mg administered subcutaneously. 7. The method of any one of claims 1-6, wherein the anti-Aβ protofibril antibody is administered at a dose of 150 mg to 200 mg, 200 mg to 250 mg, 250 mg to 300 mg, 350 mg to 400 mg, 450 mg to 500 mg, or 550 mg to 600 mg. 8. The method of any one of claims 1-7, wherein the anti-Aβ protofibril antibody is administered subcutaneously at a dose of 500 mg. 9. The method of any one of claims 1-8, wherein the dose is administered in two parts, e.g., consecutively. 10. The method of any one of claims 1-9, wherein the anti-Aβ protofibril antibody is administered once weekly. 11. The method of any one of claims 1-9, wherein the anti-Aβ protofibril antibody is administered once biweekly. 12. The method of any one of claims 1-9, wherein the anti-Aβ protofibril antibody is administered once monthly. 13. The method of any one of claims 1-12, wherein the anti-Aβ protofibril antibody is administered at an initiation dose for a first time period, e.g., according to an initiation dosing regimen, and administered at a maintenance dose for a second time period, e.g., according to a maintenance dosing regimen. 14. The method of claim 13, wherein the initiation dosing regimen comprises intravenous administration of each initiation dose or subcutaneous administration of each initiation dose. 15. The method of claim 13 or claim 14, wherein the maintenance dosing regimen comprises subcutaneous administration of each maintenance dose or intravenous administration of each maintenance dose. 16. The method of claim 13 or claim 15, wherein the initiation dosing regimen comprises at least one initiation dose administered intravenously and at least one initiation dose administered subcutaneously. 17. The method of any one of claims 13, 14, or 16, wherein the maintenance dosing regimen comprises at least one maintenance dose administered intravenously and at least one maintenance dose administered subcutaneously. Attorney Docket No.08061.0062-00304 18. The method of any one of claims 13-17, wherein the initiation dose is greater than the maintenance dose. 19. The method of claim 13, wherein the initiation dose of the anti-Aβ protofibril antibody is 150 mg to 600 mg, e.g., 200 mg to 550 mg, preferably 500 mg, administered subcutaneously. 20. The method of claim 13, wherein the maintenance dose of the anti-Aβ protofibril antibody is 150 mg to 500 mg, e.g., 360 mg, administered subcutaneously. 21. The method of claim 20, wherein the maintenance dose of the anti-Aβ protofibril antibody is 250 mg administered subcutaneously. 22. The method of any one of claims 13-21, wherein the initiation dose is administered weekly. 23. The method of any one of claims 13-22, wherein the maintenance dose is administered weekly. 24. The method of any one of claims 13-22, wherein the maintenance dose is administered biweekly. 25. The method of any one of claims 13-24, wherein the first time period is at least about 6 months, about 12 months, about 18 months, about 24 months, or about 30 months. 26. The method of claim 25, wherein the first time period is at least 18 months. 27. The method of claim 25 or claim 26, wherein the first time period is at least 24 months. 28. The method of any one of claims 13-27, wherein the first time period lasts until the subject is amyloid negative. 29. The method of claim 13, wherein the anti-Aβ protofibril antibody (e.g., BAN2401) is subcutaneously administered at an initiation dose of 500 mg weekly for at least 18 months and then subcutaneously administered at a maintenance dose of 250 mg weekly for the second period of time. 30. The method of claim 13, wherein the anti-Aβ protofibril antibody (e.g., BAN2401) is subcutaneously administered at an initiation dose of 500 mg weekly for at least 24 months, and then subcutaneously administered at a maintenance dose of 250 mg biweekly for the second period of time. 31. The method of any one of claims 13-30 wherein the second time period begins when one or more biomarkers in the subject indicate a reduction in or slowing of AD progression. 32. The method of any one of claims 13-31, wherein the second time period is at least about 6 months, about 12 months, about 18 months, about 24 months, about 36 months, about 42 months, about 48 months, about 54 months, about 60 months, or for the lifetime of the subject. 33. The method of any one of claims 13-32, wherein the maintenance dose is subcutaneously administered with an autoinjector (AI). Attorney Docket No.08061.0062-00304 34. The method of any one of claims 13-17, wherein the anti-Aβ protofibril antibody is intravenously administered at a dose of 10 mg/kg relative to the weight of the subject, biweekly. 35. The method according to any one of claims 1-34, wherein the anti-Aβ protofibril antibody is comprised in a pharmaceutical composition in the form of a pre-filled syringe. 36. The method according to any one of claims 1-34, wherein the anti-Aβ protofibril antibody is comprised in a pharmaceutical composition via an autoinjector. 37. The method according to any one of claims 1-36, wherein the anti-Aβ protofibril antibody comprising a heavy chain complementarity variable region comprising an amino acid sequence of SEQ ID NO: 1, and a light chain variable region comprising an amino acid sequence of SEQ ID NO: 2. 38. The method according to any one of claims 1-37, wherein the anti-Aβ protofibril antibody is BAN2401 (lecanemab). 39. The method of any one of claims 1-38, wherein the subject shows a change and/or difference in a measurement of one or more biomarkers associated with AD pathology prior to treatment. 40. The method of claim 39, wherein the change and/or difference in the measurement is selected from: a. increased amyloid in the brain, e.g., as measured by amyloid PET (e.g., a centiloid measure of about 20-40, e.g., a centiloid measure of about 20-32), b. increased tau in the brain, e.g., as measured by positron emission tomography (PET), c. decreased cerebrospinal fluid levels of ratio of Aβ1-42/1-40 and/or increased total tau, p- tau (e.g., p-tau181, p-tau217, and/or p-tau231), the ratio of p-tau181/np-tau181, the ratio of p- tau217/np-tau217), neurogranin, and/or neurofilament light chain (NfL), and d. decreased blood serum or plasma levels of a ratio of Aβ1-42/1-40 and/or increased total tau, phosphorylated tau (P-tau) isoforms (e.g., P-tau181, P-tau217, and/or P-tau231), ratio of p- tau181/np-tau181, the ratio of p-tau217/np-tau217, glial fibrillary acidic protein (GFAP), and/or neurofilament light chain (NfL). 41. The method of any one of claims 1-38, wherein the subject shows a change and/or difference in a measurement of one or more biomarkers associated with AD pathology during and/or after treatment. 42. The method of claim 40, wherein the change and/or difference in the measurement is selected from: Attorney Docket No.08061.0062-00304 a. decreased amyloid in the brain, e.g., as measured by amyloid PET (e.g., a centiloid measure of about 20-40, e.g., a centiloid measure of about 20-32), b. decreased tau in the brain, e.g., as measured by positron emission tomography (PET), c. increased cerebrospinal fluid levels of ratio of Aβ1-42/1-40 and/or decreased total tau, p- tau (e.g., p-tau181, p-tau217, and/or p-tau231, the ratio of p-tau181/np-tau181, the ratio of p- tau217/np-tau217), neurogranin, and/or neurofilament light chain (NfL), and d. increased blood serum or plasma levels of a ratio of Aβ1-42/1-40 and/or decreased total tau, phosphorylated tau (P-tau) isoforms (e.g., P-tau181, P-tau217, and/or P-tau231), ratio of p- tau181/np-tau181, the ratio of p-tau217/np-tau217, glial fibrillary acidic protein (GFAP), and/or neurofilament light chain (NfL). 43. The method of any one of claims 1-42, wherein the subject is amyloid-positive prior to administration, e.g., as indicated by a PET assessment, a CSF assessment of Aβ(1-42), a CSF assessment of total tau, a CSF assessment of p-tau (e.g., p-tau181, p-tau217, and/or p-tau231, the ratio of p-tau181/np-tau181, and/or the ratio of p-tau217/np-tau217), MRI, retinal amyloid accumulation, and/or a blood biomarker assessment (e.g. a plasma Aβ1-42/1-40 ratio, plasma p-tau181, plasma p- tau217, plasma p-tau 231 level, the ratio of p-tau181/np-tau181, and/or the ratio of p-tau217/np- tau217). 44. The method according to any one of claims 1-43, wherein the subject is ApoE4-positive. 45. The method of any one of claims 1-44, wherein the subject is monitored for development of ARIA. 46. The method any one of claims 1-45, wherein the subject is 65 to 80 years old. 47. The method any one of claims 1-45, wherein the subject is 55 to 64 years old and has at least one risk factor chosen from: (i) a first degree relative diagnosed with dementia onset before age 75; (ii) at least one apolipoprotein E4 variant (APOE4) allele; and (iii) elevated brain amyloid according to PET or cerebrospinal fluid (CSF) testing prior to said administration. 48. The method of any one of claims 1-47, wherein the subject has Alzheimer’s disease. 49. The method of any one of claims 1-48, wherein the subject has early Alzheimer’s disease. 50. The method of any one of claims 1-49, wherein the subject has been diagnosed with Attorney Docket No.08061.0062-00304 a. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood and/or has been diagnosed as having mild Alzheimer’s disease dementia; b. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by National Institute of Aging – Alzheimer’s Association (NIA-AA) core clinical criteria; c. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by a CDR global score of 0.5 and a Memory Box score of 0.5 or greater before treatment; d. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by a history of subjective memory decline with gradual onset and slow progression over the last 1 year before treatment, e.g., as corroborated by an informant; e. mild Alzheimer’s disease dementia by the NIA-AA core clinical criteria for probable Alzheimer’s disease dementia; or f. mild Alzheimer’s disease dementia by a CDR score of 0.5 to 1.0 and a Memory Box score of 0.5 or greater before treatment. 51. The method of any one of claims 1-47, wherein the subject is suspected of having AD. 52. The method of any one of claims 1-47, wherein the subject is a subject at risk for developing AD. 53. The method of claim 52, wherein the subject at risk for developing AD has pre-AD. 54. The method of claim 52 or claim 53, wherein the subject does not have cognitive impairment. 55. The method of any one of claims 52-54, wherein the subject has a Global Clinical Dementia Rating (CDR) score of 0 at prior to said administration. 56. The method of any one of claims 52-55, wherein the subject has a Mini-Mental State Examination (MMSE) score greater than or equal to 27, with educational adjustments, prior to said administration. 57. The method of any one of claims 52-56, wherein the subject has a Wechsler Memory Scale- Revised Logical Memory subscale II (WMS-R LM II) score prior to said administration of at least one standard deviation below age-adjusted mean in the WMS-IV LMII of less than or equal to 15 for a subject of age ranging from 50 to 64 years, of less than or equal to 12 for a subject of age ranging from 65 to 69 years, of less than or equal to 11 for a subject of age ranging from 70 to 74 years, of less than or equal to 9 for a subject of age ranging from 75 to 79 years, and of less than or equal to 7 for a subject of age ranging from 80 to 90 years. 58. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject an anti-Aβ protofibril antibody Attorney Docket No.08061.0062-00304 comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the antibody biweekly at an initiation dose of 10 mg/kg relative to the weight of the subject; and subcutaneously administering, e.g., after 18 or 24 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg. 59. A method of delaying clinical decline in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the antibody biweekly at an initiation dose of 10 mg/kg relative to the weight of the subject; and subcutaneously administering, e.g., after 18 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg. 60. A method of reducing brain amyloid level in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the antibody biweekly at an initiation dose of 10 mg/kg relative to the weight of the subject; and subcutaneously administering, e.g., after 18 or 24 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg. 61. A method of converting an amyloid positive subject to amyloid negative comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain Attorney Docket No.08061.0062-00304 complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3) , according to a dosage regimen comprising: intravenously administering the antibody biweekly at an initiation dose of 10 mg/kg relative to the weight of the subject; and subcutaneously administering, e.g., after 18 or 24 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg. 62. The method of any one of claims 58-61, wherein the initiation dose of the antibody is administered intravenously for at least 6 months, at least 12 months, at least 18 months, or at least 24 months. 63. The method of any one of claims 58-62, wherein the initiation dose of the antibody is administered intravenously for at least 18 months. 64. The method of any one of claims 58-63, wherein the initiation dose of the antibody is administered intravenously for at least 24 months. 65. The method of any one of claims 58-64, wherein the maintenance dose of the antibody is administered weekly. 66. The method of any one of claims 58-64, wherein the maintenance dose of the antibody is administered biweekly. 67. The method of any one of claims 58-66, wherein the maintenance dose of the antibody is administered using a vial-syringe. 68. The method of any one of claims 58-66, wherein the maintenance dose of the antibody is administered using an AI. 69. A method of treating Alzheimer’s disease (AD) in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: subcutaneously administering the antibody weekly at an initiation dose of 500 mg; and Attorney Docket No.08061.0062-00304 subcutaneously administering, e.g., after 18 or 24 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg. 70. A method of delaying clinical decline in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: subcutaneously administering the antibody weekly at an initiation dose of 500 mg; and subcutaneously administering, e.g., after 18 or 24 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg. 71. A method of reducing brain amyloid level in a subject having AD, suspected of having AD, or at risk for AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: subcutaneously administering the antibody weekly at an initiation dose of 500 mg; and subcutaneously administering, e.g., after 18 or 24 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg. 72. A method of converting an amyloid positive subject to amyloid negative comprising administering to the subject an antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3) , according to a dosage regimen comprising: subcutaneously administering the antibody weekly at an initiation dose of 500 mg; and subcutaneously administering, e.g., after 18 or 24 months at the initiation dose, the antibody weekly or biweekly at a maintenance dose of 250 mg. Attorney Docket No.08061.0062-00304 73. The method of any one of claims 69-72, wherein the initiation dose of the antibody is administered subcutaneously for at least 6 months, at least 12 months, at least 18 months, or at least 24 months. 74. The method of any one of claims 69-73, wherein the initiation dose of the antibody is administered subcutaneously for at least 18 months. 75. The method of any one of claims 69-73, wherein the initiation dose of the antibody is administered subcutaneously for at least 24 months. 76. The method of any one of claims 69-75, wherein the initiation dose of the antibody is administered using a vial-syringe. 77. The method of any one of claims 69-76, wherein the initiation dose of the antibody is administered using an AI. 78. The method of any one of claims 69-77, wherein the maintenance dose of the antibody is administered weekly. 79. The method of any one of claims 69-77, wherein the maintenance dose of the antibody is administered biweekly. 80. The method of any one of claims 69-79, wherein the maintenance dose of the antibody is administered using a vial-syringe. 81. The method of any one of claims 69-79, wherein the maintenance dose of the antibody is administered using an AI. 82. The method according to any one of claims 69-81, wherein the anti-Aβ protofibril antibody comprising a heavy chain complementarity variable region comprising an amino acid sequence of SEQ ID NO: 1, and a light chain variable region comprising an amino acid sequence of SEQ ID NO: 2. 83. The method according to any one of claims 69-82, wherein the anti-Aβ protofibril antibody is BAN2401 (lecanemab). 84. The method of any one of claims 69-83, wherein the subject shows a change in a measurement of one or more biomarkers associated with AD pathology prior to treatment. 85. The method of claim 84, wherein the change in the measurement is selected from: a. increased amyloid in the brain, e.g., as measured by amyloid PET (e.g., a centiloid measure of about 20-40, e.g., a centiloid measure of about 20-32), b. increased tau in the brain, e.g., as measured by positron emission tomography (PET), Attorney Docket No.08061.0062-00304 c. decreased cerebrospinal fluid levels of a ratio of Aβ1-42/1-40, and/or increased total tau, p- tau (e.g, p-tau181, p-tau217, and/or p-tau231), ratio of p-tau181/np-tau181, ratio of p-tau217/np- tau217, neurogranin, and/or neurofilament light chain (NfL), and d. decreased blood serum or plasma levels of a ratio of Aβ1-42/1-40 and/or increased total tau, phosphorylated tau (P-tau) isoforms (e.g., P-tau181, P-tau217, and/or P-tau231, ratio of p- tau181/np-tau181, ratio of p-tau217/np-tau217, glial fibrillary acidic protein (GFAP), and/or neurofilament light chain (NfL). 86. The method of any one of claims 69-84, wherein the subject shows a change and/or difference in a measurement of one or more biomarkers associated with AD pathology during and/or after treatment. 87. The method of claim 86, wherein the change and/or difference in the measurement is selected from: a. decreased amyloid in the brain, e.g., as measured by amyloid PET (e.g., a centiloid measure of about 20-40, e.g., a centiloid measure of about 20-32), b. decreased tau in the brain, e.g., as measured by positron emission tomography (PET), c. increased cerebrospinal fluid levels of ratio of Aβ1-42/1-40 and/or decreased total tau, p- tau (e.g., p-tau181, p-tau217, and/or p-tau231, the ratio of p-tau181/np-tau181, and/or the ratio of p- tau217/np-tau217), neurogranin, and/or neurofilament light chain (NfL), and d. increased blood serum or plasma levels of a ratio of Aβ1-42/1-40 and/or decreased total tau, phosphorylated tau (P-tau) isoforms (e.g., P-tau181, P-tau217, and/or P-tau231), ratio of p- tau181/np-tau181, the ratio of p-tau217/np-tau217, glial fibrillary acidic protein (GFAP), and/or neurofilament light chain (NfL). 88. The method of any one of claims 58-87 wherein the subject is amyloid-positive prior to administration, e.g., as indicated by a PET assessment, a CSF assessment of Aβ(1-42), MRI, retinal amyloid accumulation. 89. The method according to any one of claims 58-88, wherein the subject is ApoE4-positive. 90. The method of any one of claims 58-89, wherein the subject is monitored for development of ARIA. 91. The method any one of claims 58-90, wherein the subject is 65 to 80 years old. 92. The method any one of claims 58-90, wherein the subject is 55 to 64 years old and has at least one risk factor chosen from: Attorney Docket No.08061.0062-00304 (i) a first degree relative diagnosed with dementia onset before age 75; (ii) at least one apolipoprotein E4 variant (APOE4) allele; and (iii) elevated brain amyloid according to PET or cerebrospinal fluid (CSF) testing prior to said administration. 93. The method of any one of claims 58-93, wherein the subject has Alzheimer’s disease. 94. The method of any one of claims 58-93, wherein the subject has early Alzheimer’s disease. 95. The method of any one of claims 58-94, wherein the subject has been diagnosed with a. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood and/or has been diagnosed as having mild Alzheimer’s disease dementia; b. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by National Institute of Aging – Alzheimer’s Association (NIA-AA) core clinical criteria; c. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by a CDR global score of 0.5 and a Memory Box score of 0.5 or greater before treatment; d. mild cognitive impairment due to Alzheimer’s disease - intermediate likelihood by a history of subjective memory decline with gradual onset and slow progression over the last 1 year before treatment, e.g., as corroborated by an informant; e. mild Alzheimer’s disease dementia by the NIA-AA core clinical criteria for probable Alzheimer’s disease dementia; or f. mild Alzheimer’s disease dementia by a CDR score of 0.5 to 1.0 and a Memory Box score of 0.5 or greater before treatment. 96. The method of any one of claims 58-92, wherein the subject is suspected of having AD. 97. The method of any one of claims 58-92, wherein the subject is a subject at risk for developing AD. 98. The method of claim 97, wherein the subject at risk for developing AD has pre-AD. 99. The method of claim 97 or claim 98, wherein the subject does not have cognitive impairment. 100. The method of any one of claims 97-99, wherein the subject has a Global Clinical Dementia Rating (CDR) score of 0 at prior to said administration. 101. The method of any one of claims 97-100, wherein the subject has a Mini-Mental State Examination (MMSE) score greater than or equal to 27, with educational adjustments, prior to said administration. Attorney Docket No.08061.0062-00304 102. The method of any one of claims 97-101, wherein the subject has a Wechsler Memory Scale- Revised Logical Memory subscale II (WMS-R LM II) score prior to said administration of at least one standard deviation below age-adjusted mean in the WMS-IV LMII of less than or equal to 15 for a subject of age ranging from 50 to 64 years, of less than or equal to 12 for a subject of age ranging from 65 to 69 years, of less than or equal to 11 for a subject of age ranging from 70 to 74 years, of less than or equal to 9 for a subject of age ranging from 75 to 79 years, and of less than or equal to 7 for a subject of age ranging from 80 to 90 years. 103. A method of treating a subject having early AD, suspected of having early AD, or at risk for early AD, and who has received a first anti-Aβ antibody, comprising: administering to the subject a second anti-Aβ antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the second antibody biweekly or monthly at a maintenance dose of 10 mg/kg relative to the weight of the subject; or subcutaneously administering the second antibody weekly or biweekly at a maintenance dose of 250 mg. 104. A method of delaying clinical decline in a subject who has received a first anti-Aβ antibody, comprising: administering to the subject a second anti-Aβ antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the second antibody biweekly or monthly at a maintenance dose of 10 mg/kg relative to the weight of the subject; or subcutaneously administering the second antibody weekly or biweekly at a maintenance dose of 250 mg. 105. A method of reducing a brain amyloid level in a subject in a subject who has received a first anti-Aβ antibody, comprising: Attorney Docket No.08061.0062-00304 administering to the subject a second anti-Aβ antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the second antibody biweekly or monthly at a maintenance dose of 10 mg/kg relative to the weight of the subject; or subcutaneously administering the second antibody weekly or biweekly at a maintenance dose of 250 mg. 106. A method of maintaining amyloid levels in a subject who has received a first anti-Aβ antibody, comprising: administering to the subject a second anti-Aβ antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3) , according to a dosage regimen comprising: intravenously administering the second antibody biweekly or monthly at a maintenance dose of 10 mg/kg relative to the weight of the subject; or subcutaneously administering the second antibody weekly or biweekly at a maintenance dose of 250 mg. 107. A method of treating a subject having early AD, suspected of having early AD, or at risk for early AD, comprising: administering to the subject a first anti-Aβ antibody, administering to the subject a second anti-Aβ antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the second antibody biweekly or monthly at a maintenance dose of 10 mg/kg relative to the weight of the subject; or Attorney Docket No.08061.0062-00304 subcutaneously administering the second antibody weekly or biweekly at a maintenance dose, of 250 mg. 108. The method of any one of claims 103-107, wherein the subcutaneously administered maintenance dose of the antibody is administered using a vial-syringe. 109. The method of any one of claims 103-107, wherein the subcutaneously administered maintenance dose of the antibody is administered using an AI. 110. The method of any one of claims 103-109, wherein the first anti-Aβ antibody is selected from aducanumab, bapineuzumab, crenezumab, donanemab, gantenerumab, lecanemab, or solanezumab. 111. The method of claim 110, wherein the first anti-Aβ antibody is donanemab. 112. A method of treating a subject having early AD, suspected of having early AD, or at risk for early AD, comprising administering to the subject an anti-Aβ protofibril antibody comprising three heavy chain complementarity determining regions (HCDR1, HCDR2, and HCDR3) comprising amino acid sequences of SEQ ID NO: 5 (HCDR1), SEQ ID NO: 6 (HCDR2), and SEQ ID NO: 7 (HCDR3); and three light chain complementarity determining regions (LCDR1, LCDR2, and LCDR3) comprising amino acid sequences of SEQ ID NO: 8 (LCDR1), SEQ ID NO: 9 (LCDR2), and SEQ ID NO: 10 (LCDR3), according to a dosage regimen comprising: intravenously administering the antibody biweekly at a first initiation dose of 10 mg/kg relative to the weight of the subject; subcutaneously administering the antibody weekly at a second initiation dose of 720 or 500 mg; and subcutaneously administering, e.g., after 18 or 24 months of treatment on the initiation doses, the antibody weekly at a dose of 250 mg. 113. The method of any one of claims 1-112, wherein the subject is on a thrombolytic or anti- platelet agent but not an anticoagulant. 114. The method of claim 113, wherein the subject is receiving an anti-platelet medication. 115. The method of claim 113, wherein the subject is receiving a thrombolytic agent. 116. The method of claim 115, wherein the thrombolytic agent selected from the group of aspirin or a fibrinolytic agent. 117. The method of claim 116, wherein the subject is receiving aspirin. 118. The method of claim 116, wherein the subject is receiving a fibrinolytic. Attorney Docket No.08061.0062-00304 119. The method of any one of claims 1-118, wherein the subject has had or is at an increased risk for a brain hemorrhage event, e.g., a microhemorrhage or intracerebral hemorrhage, or an ARIA event, prior to treatment. 120. The method of any one of claims 1-118, wherein the subject has not had a brain hemorrhage event, e.g., a microhemorrhage or intracerebral hemorrhage, or an ARIA event, prior to treatment.