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Multiple Sclerosis and Demyelinating Pathologies: Mechanisms and Cutting-Edge Therapies, 2nd Edition
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Multiple Sclerosis and Demyelinating Pathologies: Mechanisms and Cutting-Edge Therapies, 2nd Edition

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

Deadline for manuscript submissions: 31 December 2024 | Viewed by 9342

Special Issue Editor

Dr. Elisabetta Coppi

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Guest Editor
Department of Neuroscience, Psychology, Drug Research and Child Health (NEUROFARBA), Division of Pharmacology and Toxicology, University of Florence, 50121 Florence, Italy
Interests: electrophysiology; patch clamp; synaptic transmission; long term potentiation; immunocytochemistry; oxygen glucose deprivation; myelin; oligodendrocytes; brain ischemia; multiple sclerosis; adenosine receptors
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is dedicated to the study of multiple sclerosis (MS) and other demyelinating pathologies, and will publish a collection of original research or review articles related to this topic. Highlights in the field of neuroinflammation, myelin damage, immune-mediated responses in the central nervous system (CNS), and consequent neurological deficits will be discussed. Articles should debate how these mechanisms cause or contribute to the progression of neuroinflammation and associated myelin damage or neurological symptoms, and how they might represent innovative targets for future treatments. Studies that include animal models of demyelinating pathologies (i.e., the experimental autoimmune encephalomyelitis (EAE)), the investigation of glial cells and their different roles in the pathogenesis of demyelinating diseases, research based on in vitro models of oligodendroglial/astrocyte/microglial cell cultures or co-cultures of OPC/DRG neurons as in vitro assays of de-myelination/re-myelination are highly welcome, as is research on genetic polymorphisms or epigenetic mechanisms associated with MS.

Given your profound expertise in the field, it is my pleasure and honor to invite you to contribute to this Special Issue.

If you decide to accept, I would greatly appreciate if you could send me a tentative title and a 250-word abstract summarizing your work.

Dr. Elisabetta Coppi
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

  • demyelination
  • glia
  • oligodendrocyte differentiation
  • oligodendrocyte progenitor cells
  • experimental autoimmune encephalomyelitis
  • T cells
  • autoimmunity
  • neuroinflammation
  • remyelination
  • neurobehavioral deficit
  • macrophage/microglia with matter lesion

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Related Special Issue

Published Papers (4 papers)

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Research

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16 pages, 5658 KiB  
Article
Changes in the Expression of TGF-Beta Regulatory Pathway Genes Induced by Vitamin D in Patients with Relapsing-Remitting Multiple Sclerosis
by Alberto Lozano-Ros, María L. Martínez-Ginés, José M. García-Domínguez, Sara Salvador-Martín, Haydee Goicochea-Briceño, Juan P. Cuello, Ariana Meldaña-Rivera, Yolanda Higueras-Hernández, María Sanjurjo-Sáez, Luis A. Álvarez-Sala-Walther and Luis A. López-Fernández
Int. J. Mol. Sci. 2023, 24(19), 14447; https://doi.org/10.3390/ijms241914447 - 22 Sep 2023
Cited by 2 | Viewed by 1343
Abstract
Vitamin D is an environmental factor related to multiple sclerosis that plays a significant role in immune regulation. TGF-β is a superfamily of cytokines with an important dual effect on the immune system. TGF-β inhibits the Th1 response while facilitating the preservation of [...] Read more.
Vitamin D is an environmental factor related to multiple sclerosis that plays a significant role in immune regulation. TGF-β is a superfamily of cytokines with an important dual effect on the immune system. TGF-β inhibits the Th1 response while facilitating the preservation of regulatory T cells (FOXP3+) in an immunoregulatory capacity. However, when IL-6 is present, it stimulates the Th17 response. Our aim was to analyze the regulatory effect of vitamin D on the in vivo TGF-β signaling pathway in patients with relapsing-remitting multiple sclerosis (RRMS). A total of 21 patients with vitamin D levels < 30 ng/mL were recruited and supplemented with oral vitamin D. All patients were receiving disease-modifying therapy, with the majority being on natalizumab. Expression of SMAD7, ERK1, ZMIZ1, BMP2, BMPRII, BMP4, and BMP5 was measured in CD4+ lymphocytes isolated from peripheral blood at baseline and one and six months after supplementation. SMAD7 was overexpressed at six months with respect to baseline and month one. ERK1 was overexpressed at six months with respect to month one of treatment. No significant differences in expression were observed for the remaining genes. No direct correlation was found with serum vitamin D levels. BMPRII expression changed differentially in non–natalizumab- versus natalizumab-treated patients. Changes were observed in the expression of ERK1, BMP2, and BMP5 based on disease activity measured using the Rio-Score, BMP2 in patients who had relapses, and BMP5 in those whose EDSS worsened. Our results suggest indirect regulation of vitamin D in TGF-β pathway genes in patients with RRMS. Full article
(This article belongs to the Special Issue Multiple Sclerosis and Demyelinating Pathologies: Mechanisms and Cutting-Edge Therapies, 2nd Edition)
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16 pages, 36905 KiB  
Article
The Cuprizone Mouse Model: A Comparative Study of Cuprizone Formulations from Different Manufacturers
by Malena Beecken, Louise Baumann, Elise Vankriekelsvenne, Katerina Manzhula, Theresa Greiner, Leo Heinig, Steffen Schauerte, Markus Kipp and Sarah Joost
Int. J. Mol. Sci. 2023, 24(13), 10564; https://doi.org/10.3390/ijms241310564 - 23 Jun 2023
Viewed by 2034
Abstract
The Cuprizone mouse model is widely used in studies on de- and remyelination. In the hands of different experimenters, the Cuprizone concentrations that lead to comparable levels of demyelination differ considerably. The reasons for this variability are unknown. In this study, we tested [...] Read more.
The Cuprizone mouse model is widely used in studies on de- and remyelination. In the hands of different experimenters, the Cuprizone concentrations that lead to comparable levels of demyelination differ considerably. The reasons for this variability are unknown. In this study, we tested whether different Cuprizone formulations from different vendors and manufacturers influenced Cuprizone-induced histopathological hallmarks. We intoxicated male C57BL/6 mice with six Cuprizone powders that differed in their manufacturer, vendor, and purity. After five weeks, we analyzed the body weight changes over the course of the experiment, as well as the demyelination, astrogliosis, microgliosis and axonal damage by histological LFB-PAS staining and immunohistochemical labelling of PLP, IBA1, GFAP and APP. All Cuprizone formulations induced demyelination, astrogliosis, microgliosis, axonal damage and a moderate drop in body weight at the beginning of the intoxication period. In a cumulative evaluation of all analyses, two Cuprizone formulations performed weaker than the other formulations. In conclusion, all tested formulations did work, but the choice of Cuprizone formulation may have been responsible for the considerable variability in the experimental outcomes. Full article
(This article belongs to the Special Issue Multiple Sclerosis and Demyelinating Pathologies: Mechanisms and Cutting-Edge Therapies, 2nd Edition)
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Review

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15 pages, 657 KiB  
Review
The Role of Selected Interleukins in the Development and Progression of Multiple Sclerosis—A Systematic Review
by Cezary Grunwald, Anna Krętowska-Grunwald, Edyta Adamska-Patruno, Jan Kochanowicz, Alina Kułakowska and Monika Chorąży
Int. J. Mol. Sci. 2024, 25(5), 2589; https://doi.org/10.3390/ijms25052589 - 23 Feb 2024
Cited by 4 | Viewed by 2022
Abstract
Multiple sclerosis is a disabling inflammatory disorder of the central nervous system characterized by demyelination and neurodegeneration. Given that multiple sclerosis remains an incurable disease, the management of MS predominantly focuses on reducing relapses and decelerating the progression of both physical and cognitive [...] Read more.
Multiple sclerosis is a disabling inflammatory disorder of the central nervous system characterized by demyelination and neurodegeneration. Given that multiple sclerosis remains an incurable disease, the management of MS predominantly focuses on reducing relapses and decelerating the progression of both physical and cognitive decline. The continuous autoimmune process modulated by cytokines seems to be a vital contributing factor to the development and relapse of multiple sclerosis. This review sought to summarize the role of selected interleukins in the pathogenesis and advancement of MS. Patients with MS in the active disease phase seem to exhibit an increased serum level of IL-2, IL-4, IL-6, IL-13, IL-17, IL-21, IL-22 and IL-33 compared to healthy controls and patients in remission, while IL-10 appears to have a beneficial impact in preventing the progression of the disease. Despite being usually associated with proinflammatory activity, several studies have additionally recognized a neuroprotective role of IL-13, IL-22 and IL-33. Moreover, selected gene polymorphisms of IL-2R, IL-4, IL-6, IL-13 and IL-22 were identified as a possible risk factor related to MS development. Treatment strategies of multiple sclerosis that either target or utilize these cytokines seem rather promising, but more comprehensive research is necessary to gain a clearer understanding of how these cytokines precisely affect MS development and progression. Full article
(This article belongs to the Special Issue Multiple Sclerosis and Demyelinating Pathologies: Mechanisms and Cutting-Edge Therapies, 2nd Edition)
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25 pages, 2735 KiB  
Review
An Elusive Target: Inhibitors of JC Polyomavirus Infection and Their Development as Therapeutics for the Treatment of Progressive Multifocal Leukoencephalopathy
by Jacob Kaiserman, Bethany A. O’Hara, Sheila A. Haley and Walter J. Atwood
Int. J. Mol. Sci. 2023, 24(10), 8580; https://doi.org/10.3390/ijms24108580 - 11 May 2023
Cited by 6 | Viewed by 3393
Abstract
Progressive multifocal leukoencephalopathy (PML) is a rare demyelinating disease caused by infection with JC Polyomavirus (JCPyV). Despite the identification of the disease and isolation of the causative pathogen over fifty years ago, no antiviral treatments or prophylactic vaccines exist. Disease onset is usually [...] Read more.
Progressive multifocal leukoencephalopathy (PML) is a rare demyelinating disease caused by infection with JC Polyomavirus (JCPyV). Despite the identification of the disease and isolation of the causative pathogen over fifty years ago, no antiviral treatments or prophylactic vaccines exist. Disease onset is usually associated with immunosuppression, and current treatment guidelines are limited to restoring immune function. This review summarizes the drugs and small molecules that have been shown to inhibit JCPyV infection and spread. Paying attention to historical developments in the field, we discuss key steps of the virus lifecycle and antivirals known to inhibit each event. We review current obstacles in PML drug discovery, including the difficulties associated with compound penetrance into the central nervous system. We also summarize recent findings in our laboratory regarding the potent anti-JCPyV activity of a novel compound that antagonizes the virus-induced signaling events necessary to establish a productive infection. Understanding the current panel of antiviral compounds will help center the field for future drug discovery efforts. Full article
(This article belongs to the Special Issue Multiple Sclerosis and Demyelinating Pathologies: Mechanisms and Cutting-Edge Therapies, 2nd Edition)
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