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Molecular Mechanism in Multiple Sclerosis and Related Disorders 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 28 June 2024 | Viewed by 1332

Special Issue Editors


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Guest Editor
1. Department of Neurology, Heinrich-Heine-University Düsseldorf, D-40225 Dusseldorf, Germany
2. Brain and Mind Center, University of Sydney, Sydney, NSW 2050, Australia
Interests: interferon; virus; immunology multiple sclerosis neuroimmunology
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Guest Editor
1. Department of Neurorehabilitation Sciences, Casa di Cura Igea, 20132 Milan, Italy
2. Vita-Salute San Raffaele University, 20132 Milan, Italy
Interests: multiple sclerosis treatment; monitoring; epidemiology
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Guest Editor
1. Department of Multiple Sclerosis Therapeutics, Fukushima Medical University, Fukushima, Japan
2. Multiple Sclerosis & Neuromyelitis Optica Center, Southern TOHOKU Research Institute for Neuroscience, Koriyama, Japan
Interests: multiple sclerosis; neuromyelitis optica spectrum disorder; MOG antibody-associated disease

Special Issue Information

Dear Colleagues,

Immune mediated inflammatory demyelinating central nervous disease include multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSDs), anti Myelin Oligodendrocytes Antibody Associated Disease (MOGAD), and some other rare disorders. The aim of this special issue is to explore mechanistic aspects of these disorders which are now better defined. Nevertheless, there are still a number of unresolved issues. A special focus will be on pathways underlying the neurodegenerative phase of MS, the role of innate immune cells, of persistent demyelination and of iron toxicity. We are also interested to collect contributions in the area of body fluid, imaging and functional biomarkers connected with specific pathophysiological mechanisms and activity and stages of the disease. Very welcome are contributions on animal models of these disorders, including models of demyelination/remyelination. Finally, new disease modifying treatments for MS and related disorders, both with an antinflammatory profile and neuroprotective mode of action are under the scope of this special issue.

Prof. Dr. Hans-Peter Hartung
Prof. Dr. Giancarlo Comi
Prof. Dr. Kazuo Fujihara
Guest Editors

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
  • NMOSD
  • MOGAD
  • disease modifying treatments

Published Papers (1 paper)

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Research

15 pages, 2220 KiB  
Article
Tissue Hypoxia and Associated Innate Immune Factors in Experimental Autoimmune Optic Neuritis
by Zhiyuan Yang, Cristina Marcoci, Hatice Kübra Öztürk, Eleni Giama, Ayse Gertrude Yenicelik, Ondřej Slanař, Christopher Linington, Roshni Desai and Kenneth J. Smith
Int. J. Mol. Sci. 2024, 25(5), 3077; https://doi.org/10.3390/ijms25053077 - 06 Mar 2024
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Abstract
Visual loss in acute optic neuritis is typically attributed to axonal conduction block due to inflammatory demyelination, but the mechanisms remain unclear. Recent research has highlighted tissue hypoxia as an important cause of neurological deficits and tissue damage in both multiple sclerosis (MS) [...] Read more.
Visual loss in acute optic neuritis is typically attributed to axonal conduction block due to inflammatory demyelination, but the mechanisms remain unclear. Recent research has highlighted tissue hypoxia as an important cause of neurological deficits and tissue damage in both multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE) and, here, we examine whether the optic nerves are hypoxic in experimental optic neuritis induced in Dark Agouti rats. At both the first and second peaks of disease expression, inflamed optic nerves labelled significantly for tissue hypoxia (namely, positive for hypoxia inducible factor-1α (HIF1α) and intravenously administered pimonidazole). Acutely inflamed nerves were also labelled significantly for innate markers of oxidative and nitrative stress and damage, including superoxide, nitric oxide and 3-nitrotyrosine. The density and diameter of capillaries were also increased. We conclude that in acute optic neuritis, the optic nerves are hypoxic and come under oxidative and nitrative stress and damage. Tissue hypoxia can cause mitochondrial failure and thus explains visual loss due to axonal conduction block. Tissue hypoxia can also induce a damaging oxidative and nitrative environment. The findings indicate that treatment to prevent tissue hypoxia in acute optic neuritis may help to restore vision and protect from damaging reactive oxygen and nitrogen species. Full article
(This article belongs to the Special Issue Molecular Mechanism in Multiple Sclerosis and Related Disorders 2.0)
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