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Prevention, Intervention and Care of Neurodegenerative Diseases: Second Edition
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Prevention, Intervention and Care of Neurodegenerative Diseases: Second Edition

A special issue of Healthcare (ISSN 2227-9032). This special issue belongs to the section "Chronic Care".

Deadline for manuscript submissions: closed (31 December 2024) | Viewed by 2672

Special Issue Editor

Dr. Christos Bakirtzis

E-Mail Website
Guest Editor
University General Hospital of Thessaloniki "AHEPA", Thessaloniki, Greece
Interests: neuroimaging; cognition; multiple sclerosis; neuroimmunology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Our current ability to detect neurodegenerative diseases early and manage them is limited. The insidious processes underlying these conditions are only partly understood, while the treatments used have limited efficacies. Current research aims to understand the mechanisms underlying the progressive axonal loss in various neurologic conditions and seeks ways to properly monitor, quantify, and treat their relevant clinical implications. 

This Special Issue of Healthcare seeks commentaries, original research, short reports, and reviews focusing on challenges in detecting, monitoring, and treating neurodegenerative diseases. This Special Issue aims to provide information about advances in the research of various primarily neurodegenerative conditions such as dementia, Parkinson’s Disease, motor neurone disease, and diseases with evident neurodegenerative components such as multiple sclerosis.

Dr. Christos Bakirtzis
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Healthcare is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • neurodegeneration
  • axonal loss

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Related Special Issue

Published Papers (1 paper)

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Review

14 pages, 3077 KiB  
Review
The Time Trajectory of Choroid Plexus Enlargement in Multiple Sclerosis
by Athina Andravizou, Sotiria Stavropoulou De Lorenzo, Evangelia Kesidou, Iliana Michailidou, Dimitrios Parissis, Marina-Kleopatra Boziki, Polyxeni Stamati, Christos Bakirtzis and Nikolaos Grigoriadis
Healthcare 2024, 12(7), 768; https://doi.org/10.3390/healthcare12070768 - 1 Apr 2024
Cited by 2 | Viewed by 2200
Abstract
Choroid plexus (CP) can be seen as a watchtower of the central nervous system (CNS) that actively regulates CNS homeostasis. A growing body of literature suggests that CP alterations are involved in the pathogenesis of multiple sclerosis (MS) but the underlying mechanisms remain [...] Read more.
Choroid plexus (CP) can be seen as a watchtower of the central nervous system (CNS) that actively regulates CNS homeostasis. A growing body of literature suggests that CP alterations are involved in the pathogenesis of multiple sclerosis (MS) but the underlying mechanisms remain elusive. CPs are enlarged and inflamed in relapsing-remitting (RRMS) but also in clinically isolated syndrome (CIS) and radiologically isolated syndrome (RIS) stages, far beyond MS diagnosis. Increases in the choroid plexus/total intracranial volume (CP/TIV) ratio have been robustly associated with increased lesion load, higher translocator protein (TSPO) uptake in normal-appearing white matter (NAWM) and thalami, as well as with higher annual relapse rate and disability progression in highly active RRMS individuals, but not in progressive MS. The CP/TIV ratio has only slightly been correlated with magnetic resonance imaging (MRI) findings (cortical or whole brain atrophy) and clinical outcomes (EDSS score) in progressive MS. Therefore, we suggest that plexus volumetric assessments should be mainly applied to the early disease stages of MS, whereas it should be taken into consideration with caution in progressive MS. In this review, we attempt to clarify the pathological significance of the temporal CP volume (CPV) changes in MS and highlight the pitfalls and limitations of CP volumetric analysis. Full article
(This article belongs to the Special Issue Prevention, Intervention and Care of Neurodegenerative Diseases: Second Edition)
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Figure 1

Figure 1
<p>The architecture of the choroid plexus. Normally, the choroid plexus is an active regulator of CNS homeostasis by producing CSF and regulating the immune cell trafficking into the brain parenchyma. Immune cells reside in the plexus stroma, mostly epiplexus macrophages (or Kolmer cells), which project between the epithelial cells, and dendritic cells. The blood–CSF barrier (or plexus epithelium) tightly regulates the passage of molecules and solutes from the systemic circulation into the CNS. (CNS: Central Nervous System, CSF: Cerebrospinal fluid, FGF-2: Fibroblast growth factor-2, GDF-15: Growth/differentiation factor 15, MIC-1: macrophage inhibitory cytokine 1, TGT-1β-3: Tissue Growth Factor-1β-3.) Created with BioRender.com.</p> Full article ">Figure 2
<p>Acute inflammation and choroid plexus edema (enlargement): In the inflammatory phases of the disease, general inflammation leads to demyelination. The choroid plexus endothelium recruits pro-inflammatory CD4+ T cells through the upregulation of adhesion molecules such as VCAM1. The accumulation of the plexus stroma with T cells leads to swelling of the plexus (local edema), while immune cells cross the plexus epithelium (and the permissive ependyma) into the brain parenchyma. (BCSFB: Blood cerebrospinal fluid barrier, BBB: Blood–brain barrier, IL: Interleukin. VCAM-1: Vascular cell adhesion molecule 1). Created with BioRender.com.</p> Full article ">Figure 3
<p>Chronic inflammation and choroid plexus hypoxia. In progressive MS (either secondary or primary progressive), inflammation is mild, and neurodegeneration prevails. Damage signals from the brain, such as ROS and iNOS, leak through the ependymal cells, into the ventricular CSF, towards the choroid plexus. These signals lead to oxidative stress, activation of the HIF 1 signaling pathway, and virtual hypoxia at the plexus. The BCSFB and the BBB are intact or restored. In response to chronic intrathecal inflammation and ROS, the plexus produces cytokines, leading to the recruitment of granulocytes and neutrophils, which further contribute to inflammatory cytokines secretion. T cells, particularly the CD8 subset, also accumulate in the plexus stroma, together with NK cells through the blood–brain barrier, into the CSF, towards the periventricular brain tissue. (MS: Multiple Sclerosis, CSF: Cerebrospinal Fluid, BCSFB: Blood cerebrospinal fluid barrier, BBB: Blood–brain barrier, NK: Natural Killer, CP: Choroid Plexus, ROS: Reactive oxygen species iNOS: Inducible nitric oxide synthetase, HIF-1: hypoxia-induced factor 1). Created with BioRender.com.</p> Full article ">
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