Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.1
4.9
Journals
IJMS
Special Issues
Multiple Sclerosis at the Crossroads of Autoimmunity and Neurodegeneration 2.0
ijms-logo
Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Multiple Sclerosis at the Crossroads of Autoimmunity and Neurodegeneration 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: closed (31 October 2024) | Viewed by 3072

Special Issue Editor

Prof. Dr. Serge Nataf

E-Mail Website
Guest Editor
1. Bank of Tissues and Cells, Hospices Civils de Lyon, Hôpital Edouard Herriot, Place d’Arsonval, F-69003 Lyon, France
2. Stem-Cell and Brain Research Institute, 18 Avenue du Doyen Lépine, F-69500 Bron, France
3. Lyon-Est School of Medicine, University Claude Bernard Lyon 1, 43 Bd du 11 Novembre 1918, F-69100 Villeurbanne, France
Interests: multiple sclerosis pathophysiology; CNS-targeted autoimmunity; neuroinflammation; computational data mining; systems biology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is the continuation of our previous Special Issue, “Multiple Sclerosis at the Crossroads of Autoimmunity and Neurodegeneration”.

There is increasing evidence that the slowly evolving disability in multiple sclerosis (MS) patients is, at least in part, disconnected from relapses. Recent findings indicate that, in addition to the well-recognized progressive forms of MS, a steady aggravation of neurological deficits may also occur in patients suffering from relapsing–remitting MS. Such a clinical progression is silent (i.e., independent from both clinical relapses and brain radiological activity) and was found to be closely associated with the rate of cervical spinal cord atrophy. While neurodegeneration in MS is usually thought to result from decades-long neuroinflammatory processes, these observations indicate that autoimmunity and neurodegeneration may actually develop concurrently. This Special Issue aims to provide an updated overview of our knowledge of the links between autoimmunity and neurodegeneration in MS. All papers relating to the general topic of this Special Issue will be considered. However, we specifically encourage the submission of articles addressing one or several of the following issues in the context of MS or related disorders:

  1. Neuronal target antigens in MS and/or its animal model (experimental autoimmune encephalomyelitis);
  2. Mechanisms favoring the intrathecal persistence of autoreactive lymphocytes;
  3. Pro-degenerative vs. pro-regenerative impact of molecules involved in the resolution of CNS acute inflammation;
  4. Insights into the mechanisms of inflammation-associated axonal loss and/or synaptic pruning.

Prof. Dr. Serge Nataf
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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
  • multiple sclerosis
  • autoimmunity
  • T lymphocytes
  • B lymphocytes
  • demyelination
  • axonal loss
  • synaptic pruning
  • microglia
  • astrocytes

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Published Papers (2 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

14 pages, 1006 KiB  
Article
The Immunometabolic Gene N-Acetylglucosamine Kinase Is Uniquely Involved in the Heritability of Multiple Sclerosis Severity
by Serge Nataf, Marine Guillen and Laurent Pays
Int. J. Mol. Sci. 2024, 25(7), 3803; https://doi.org/10.3390/ijms25073803 - 28 Mar 2024
Cited by 1 | Viewed by 1382
Abstract
The clinical severity of multiple sclerosis (MS), an autoimmune disorder of the central nervous system, is thought to be determined by environmental and genetic factors that have not yet been identified. In a recent genome-wide association study (GWAS), a single nucleotide polymorphism (SNP), [...] Read more.
The clinical severity of multiple sclerosis (MS), an autoimmune disorder of the central nervous system, is thought to be determined by environmental and genetic factors that have not yet been identified. In a recent genome-wide association study (GWAS), a single nucleotide polymorphism (SNP), rs10191329, has been associated with MS severity in two large independent cohorts of patients. Different approaches were followed by the authors to prioritize the genes that are transcriptionally regulated by such an SNP. It was concluded that the identified SNP regulates a group of proximal genes involved in brain resilience and cognitive abilities rather than immunity. Here, by conducting an alternative strategy for gene prioritization, we reached the opposite conclusion. According to our re-analysis, the main target of rs10191329 is N-Acetylglucosamine Kinase (NAGK), a metabolic gene recently shown to exert major immune functions via the regulation of the nucleotide-binding oligomerization domain-containing protein 2 (NOD2) pathway. To gain more insights into the immunometabolic functions of NAGK, we analyzed the currently known list of NAGK protein partners. We observed that NAGK integrates a dense network of human proteins that are involved in glucose metabolism and are highly expressed by classical monocytes. Our findings hold potentially major implications for the understanding of MS pathophysiology. Full article
(This article belongs to the Special Issue Multiple Sclerosis at the Crossroads of Autoimmunity and Neurodegeneration 2.0)
►▼ Show Figures

Figure 1

9 pages, 505 KiB  
Communication
No Association of Multiple Sclerosis with C9orf72 Hexanucleotide Repeat Size in an Austrian Cohort
by Theresa König, Fritz Leutmezer, Thomas Berger, Alexander Zimprich, Christiane Schmied, Elisabeth Stögmann and Tobias Zrzavy
Int. J. Mol. Sci. 2023, 24(14), 11254; https://doi.org/10.3390/ijms241411254 - 9 Jul 2023
Viewed by 1220
Abstract
Multiple Sclerosis (MS) is a common immune-mediated disorder of the central nervous system that affects young adults and is characterized by demyelination and neurodegeneration. Recent studies have associated C9orf72 intermediate repeat expansions with MS. The objective of this study was to investigate whether [...] Read more.
Multiple Sclerosis (MS) is a common immune-mediated disorder of the central nervous system that affects young adults and is characterized by demyelination and neurodegeneration. Recent studies have associated C9orf72 intermediate repeat expansions with MS. The objective of this study was to investigate whether C9orf72 repeat length is associated with MS or with a specific disease course in a monocentric Austrian MS cohort. Genotyping of 382 MS patients and 643 non-neurological controls for C9orf72 repeat expansions was performed. The study did not find a difference in the distribution of repeat numbers between controls and MS cases (median repeat units = 2; p = 0.39). Additionally, sub-analysis did not establish a link between intermediate repeats and MS (p = 0.23) and none of the patients with progressive disease course carried an intermediate allele (20–30 repeat units). Exploratory analysis for different cut-offs (of ≥7, ≥17, and ≥24) did not reveal any significant differences in allele frequencies between MS and controls. However, the study did identify a progressive MS patient with a pathogenic C9orf72 expansion and probable co-existing behavioral variant frontotemporal dementia (bvFTD) in a retrospective chart review. In conclusion, this study did not find evidence supporting an association between C9orf72 repeat length and MS or a specific disease course in the Austrian MS cohort. However, the identification of a progressive MS patient with a pathogenic C9orf72 expansion and probable co-existing with FTD highlights the complexity and challenges involved in recognizing distinct neurodegenerative diseases that may co-occur in MS patients. Full article
(This article belongs to the Special Issue Multiple Sclerosis at the Crossroads of Autoimmunity and Neurodegeneration 2.0)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-2
Back to TopTop