Transgenic mice with Alzheimer presenilin 1 mutations show accelerated neurodegeneration without amyloid plaque formation. (Q53335187)

13 May 2018

title

Transgenic mice with Alzheimer presenilin 1 mutations show accelerated neurodegeneration without amyloid plaque formation. (English)

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13 May 2018

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Chui DH

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13 May 2018

Tanahashi H

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13 May 2018

Ozawa K

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13 May 2018

Ikeda S

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13 May 2018

Checler F

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13 May 2018

Ueda O

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13 May 2018

Suzuki H

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13 May 2018

Araki W

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13 May 2018

Inoue H

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13 May 2018

Shirotani K

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13 May 2018

Takahashi K

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13 May 2018

Gallyas F

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13 May 2018

Tabira T

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13 May 2018

language of work or name

English

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publication date

1 May 1999

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13 May 2018

published in

Nature Medicine

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13 May 2018

volume

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13 May 2018

issue

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13 May 2018

page(s)

560-564

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13 May 2018

Cloning of a gene bearing missense mutations in early-onset familial Alzheimer's disease

cites work

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Presenilin mutations in Alzheimer's disease

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Familial Alzheimer's disease genes in Japanese.

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Secreted amyloid beta-protein similar to that in the senile plaques of Alzheimer's disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer's disease

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The E280A presenilin 1 Alzheimer mutation produces increased A beta 42 deposition and severe cerebellar pathology

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Increased amyloid-beta42(43) in brains of mice expressing mutant presenilin 1

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7 January 2021

Familial Alzheimer's disease-linked presenilin 1 variants elevate Abeta1-42/1-40 ratio in vitro and in vivo

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7 January 2021

Mutant presenilins of Alzheimer's disease increase production of 42-residue amyloid beta-protein in both transfected cells and transgenic mice

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7 January 2021

Alzheimer's presenilin mutation sensitizes neural cells to apoptosis induced by trophic factor withdrawal and amyloid beta-peptide: involvement of calcium and oxyradicals.

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7 January 2021

Participation of presenilin 2 in apoptosis: enhanced basal activity conferred by an Alzheimer mutation

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Four modified silver methods for thick sections of formaldehyde-fixed mammalian central nervous tissue: 'dark' neurons, perikarya of all neurons, microglial cells and capillaries

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Formation of "dark" (argyrophilic) neurons of various origin proceeds with a common mechanism of biophysical nature (a novel hypothesis).

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Amyloid, the presenilins and Alzheimer's disease

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7 January 2021

Alzheimer's disease: a re-examination of the amyloid hypothesis

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Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein

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APPSw transgenic mice develop age-related A beta deposits and neuropil abnormalities, but no neuronal loss in CA1.

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7 January 2021

Accelerated amyloid deposition in the brains of transgenic mice coexpressing mutant presenilin 1 and amyloid precursor proteins

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7 January 2021

Accelerated Alzheimer-type phenotype in transgenic mice carrying both mutant amyloid precursor protein and presenilin 1 transgenes

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Neuron loss in APP transgenic mice

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Proteolytic processing of Alzheimer's disease associated proteins.

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Destabilization of beta-catenin by mutations in presenilin-1 potentiates neuronal apoptosis

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Aging renders the brain vulnerable to amyloid beta-protein neurotoxicity

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A variant of Alzheimer's disease with spastic paraparesis and unusual plaques due to deletion of exon 9 of presenilin 1.

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Stress induces neuronal death in the hippocampus of castrated rats

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Neuronal and glial apoptosis after traumatic spinal cord injury.

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Characterization of new polyclonal antibodies specific for 40 and 42 amino acid-long amyloid beta peptides: their use to examine the cell biology of presenilins and the immunohistochemistry of sporadic Alzheimer's disease and cerebral amyloid angiop

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Immunohistochemical study of Alzheimer's disease using antibodies to synthetic amyloid and fibronectin

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Identifiers

DOI

10.1038/8438

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13 May 2018

release_4k76yfrhtrgatmeysumiivjp24

Fatcat ID

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Fatcat

https://api.fatcat.wiki/v0/release/4k76yfrhtrgatmeysumiivjp24

24 November 2022

mapped directly with Wikidata item

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13 May 2018