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Demyelinating Diseases: From Molecular Mechanisms to, Therapeutic Strategies—3rd Edition
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Demyelinating Diseases: From Molecular Mechanisms to, Therapeutic Strategies—3rd 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 July 2024 | Viewed by 4057

Special Issue Editor

Dr. Antonietta Bernardo

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Guest Editor
National Center for Drug Research and Evaluation, Istituto Superiore di Sanità, Viale Regina Elena, 299, 00161 Rome, Italy
Interests: neuroscience; neurodegenerative disease; myelination and remyelination; oligodendrocytes; signal transduction
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This is the third Special Issue in the continued series focused on the hot topic of demyelinating diseases. We have already launched two successful Special Issues which received interesting contributions and discussions (https://www.mdpi.com/journal/ijms/special_issue/demyelinating_diseases; https://www.mdpi.com/journal/ijms/special_issues/HZ6L4ZMBB7).

Demyelinating diseases are a group of pathologies characterized by the alteration of myelin, that is, the coating that wraps most of the nerve fibers of the central and peripheral nervous system, whose goal is to improve nerve conduction and the preservation of energy spent during action potential propagation. They are very disabling diseases, affecting millions of people worldwide. There are different types of demyelinating disorders, each characterized by peculiar characteristics that allow for their classification. A broad classification of demyelinating diseases is drawn according to their pathogenesis, including the following categories: due to immune-mediated inflammatory processes, infectious diseases, caused by metabolic disorders, and hypoxic-ischaemic forms. The myelin produced by oligodendrocytes in the central nervous system (CNS) differs in terms of chemical and immunological features from that provided in the peripheral nervous system (PNS) by Schwann cells. Accordingly, some demyelinating diseases mainly affect the peripheral nerves, while others primarily affect the CNS. In most cases, however, there is no effective pharmacological treatment capable of completely restoring the normal functionality of myelin and nerve conduction.

The aim of this Special Issue, entitled “Demyelinating Diseases: From Molecular Mechanisms to, Therapeutic Strategies 3.0”, is dual: to offer an overview on the landscape of research devoted to deepening knowledge on the pathogenic mechanisms involved in demyelinating diseases and to gather an ensemble of the efforts aimed at the identification and pre-clinical validation of targets for therapeutic approaches to be utilized in preventive or curing strategies to improve the quality of life of patients suffering from these severe pathologies. Experimental papers on in vitro or ex vivo models, up-to-date review articles, and commentaries are all welcome.

Dr. Antonietta Bernardo
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

  • biomarkers
  • cellular and molecular biology
  • cell differentiation
  • cellular metabolism
  • demyelinating diseases
  • drug developing strategies and drug repositioning
  • glia cell (oligodendrocytes, astrocytes and microglia)
  • inflammation
  • lipid metabolism
  • mitochondria
  • myelination and remyelination nuclear receptors
  • nutraceuticals
  • signal transduction mechanisms
  • target identification

Published Papers (3 papers)

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Research

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25 pages, 12637 KiB  
Article
Exploring the Role of Platelets in Virus-Induced Inflammatory Demyelinating Disease and Myocarditis
by Ijaz Ahmad, Seiichi Omura, Fumitaka Sato, Ah-Mee Park, Sundar Khadka, Felicity N. E. Gavins, Hiroki Tanaka, Motoko Y. Kimura and Ikuo Tsunoda
Int. J. Mol. Sci. 2024, 25(6), 3460; https://doi.org/10.3390/ijms25063460 - 19 Mar 2024
Viewed by 1656
Abstract
Theiler’s murine encephalomyelitis virus (TMEV) infection has been used as a mouse model for two virus-induced organ-specific immune-mediated diseases. TMEV-induced demyelinating disease (TMEV-IDD) in the central nervous system (CNS) is a chronic inflammatory disease with viral persistence and an animal model of multiple [...] Read more.
Theiler’s murine encephalomyelitis virus (TMEV) infection has been used as a mouse model for two virus-induced organ-specific immune-mediated diseases. TMEV-induced demyelinating disease (TMEV-IDD) in the central nervous system (CNS) is a chronic inflammatory disease with viral persistence and an animal model of multiple sclerosis (MS) in humans. TMEV infection can also cause acute myocarditis with viral replication and immune cell infiltration in the heart, leading to cardiac fibrosis. Since platelets have been reported to modulate immune responses, we aimed to determine the role of platelets in TMEV infection. In transcriptome analyses of platelets, distinct sets of immune-related genes, including major histocompatibility complex (MHC) class I, were up- or downregulated in TMEV-infected mice at different time points. We depleted platelets from TMEV-infected mice by injecting them with platelet-specific antibodies. The platelet-depleted mice had significantly fewer viral antigen-positive cells in the CNS. Platelet depletion reduced the severities of TMEV-IDD and myocarditis, although the pathology scores did not reach statistical significance. Immunologically, the platelet-depleted mice had an increase in interferon (IFN)-γ production with a higher anti-TMEV IgG2a/IgG1 ratio. Thus, platelets may play roles in TMEV infection, such as gene expression, viral clearance, and anti-viral antibody isotype responses. Full article
(This article belongs to the Special Issue Demyelinating Diseases: From Molecular Mechanisms to, Therapeutic Strategies—3rd Edition)
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Review

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27 pages, 1342 KiB  
Review
Macrophages and HLA-Class II Alleles in Multiple Sclerosis: Insights in Therapeutic Dynamics
by Petros Prapas and Maria Anagnostouli
Int. J. Mol. Sci. 2024, 25(13), 7354; https://doi.org/10.3390/ijms25137354 - 4 Jul 2024
Viewed by 585
Abstract
Antigen presentation is a crucial mechanism that drives the T cell-mediated immune response and the development of Multiple Sclerosis (MS). Genetic alterations within the highly variable Major Histocompatibility Complex Class II (MHC II) have been proven to result in significant changes in the [...] Read more.
Antigen presentation is a crucial mechanism that drives the T cell-mediated immune response and the development of Multiple Sclerosis (MS). Genetic alterations within the highly variable Major Histocompatibility Complex Class II (MHC II) have been proven to result in significant changes in the molecular basis of antigen presentation and the clinical course of patients with both Adult-Onset MS (AOMS) and Pediatric-Onset MS (POMS). Among the numerous polymorphisms of the Human Leucocyte Antigens (HLA), within MHC II complex, HLA-DRB1*15:01 has been labeled, in Caucasian ethnic groups, as a high-risk allele for MS due to the ability of its structure to increase affinity to Myelin Basic Protein (MBP) epitopes. This characteristic, among others, in the context of the trimolecular complex or immunological synapsis, provides the foundation for autoimmunity triggered by environmental or endogenous factors. As with all professional antigen presenting cells, macrophages are characterized by the expression of MHC II and are often implicated in the formation of MS lesions. Increased presence of M1 macrophages in MS patients has been associated both with progression and onset of the disease, each involving separate but similar mechanisms. In this critical narrative review, we focus on macrophages, discussing how HLA genetic alterations can promote dysregulation of this population’s homeostasis in the periphery and the Central Nervous System (CNS). We also explore the potential interconnection in observed pathological macrophage mechanisms and the function of the diverse structure of HLA alleles in neurodegenerative CNS, seen in MS, by comparing available clinical with molecular data through the prism of HLA-immunogenetics. Finally, we discuss available and experimental pharmacological approaches for MS targeting the trimolecular complex that are based on cell phenotype modulation and HLA genotype involvement and try to reveal fertile ground for the potential development of novel drugs. Full article
(This article belongs to the Special Issue Demyelinating Diseases: From Molecular Mechanisms to, Therapeutic Strategies—3rd Edition)
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17 pages, 1474 KiB  
Review
The Immunomodulatory Potential of Short-Chain Fatty Acids in Multiple Sclerosis
by Laura Barcutean, Smaranda Maier, Mihai Burai-Patrascu, Lenard Farczadi and Rodica Balasa
Int. J. Mol. Sci. 2024, 25(6), 3198; https://doi.org/10.3390/ijms25063198 - 11 Mar 2024
Viewed by 1491
Abstract
Multiple sclerosis (MS) is a chronic inflammatory and neurodegenerative central nervous system (CNS) disorder, characterized by focal inflammation, demyelination, irreversible axonal loss and neurodegeneration. The proposed mechanism involves auto-reactive T lymphocytes crossing the blood–brain barrier (BBB), contributing to inflammation and demyelination. Pro-inflammatory Th1 [...] Read more.
Multiple sclerosis (MS) is a chronic inflammatory and neurodegenerative central nervous system (CNS) disorder, characterized by focal inflammation, demyelination, irreversible axonal loss and neurodegeneration. The proposed mechanism involves auto-reactive T lymphocytes crossing the blood–brain barrier (BBB), contributing to inflammation and demyelination. Pro-inflammatory Th1 and Th17 lymphocytes are pivotal in MS pathogenesis, highlighting an imbalanced interaction with regulatory T cells. Dysbiosis in the gut microbiota, characterized by microbial imbalance is implicated in systemic inflammation, yet its exact role in MS remains elusive. Short-chain fatty acids (SCFAs), including valerate, butyrate, propionate, and acetate, produced through dietary fiber fermentation by the gut microbiota, modulate inflammation and immune responses. Particularly, butyrate and propionate exhibit pronounced anti-inflammatory effects in both the gut and CNS. These SCFAs influence regulatory T lymphocyte expression and BBB permeability. This review discusses the potential therapeutic implications of SCFA in MS, highlighting their ability to modulate the gut–brain axis and restore immune balance. Full article
(This article belongs to the Special Issue Demyelinating Diseases: From Molecular Mechanisms to, Therapeutic Strategies—3rd Edition)
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