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Molecular Advances and Perspectives in Multiple Sclerosis

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: 20 December 2024 | Viewed by 718

Special Issue Editors


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Guest Editor
Inflammation at the Nervous System Interfaces Research Line, Centro Clínico Académico Braga Associação, School of Medicine, University of Minho, 4710-057 Braga, Portugal
Interests: multiple sclerosis; cognition; EBV; CSF

E-Mail
Guest Editor
Inflammation at the Nervous System Interfaces Research Line, Centro Clínico Académico Braga Associação, School of Medicine, University of Minho, 4710-057 Braga, Portugal
Interests: experimental autoimmune encephalomielitis; immunometabolism; glial cells; brain barriers; CSF; lipocalin 2

Special Issue Information

Dear Colleagues,

Multiple sclerosis is an auto-immune disease affecting the central nervous system that has both demyelinating and neurodegeneration components. Despite the availability of high efficacy treatments, the pathophysiology of the disease remains poorly understood and many patients still experience disability progression in the long term. In recent years, there have been many new insights into the triggers of the disease (with a focus on Epstein–Barr virus infection) and the drivers of chronic inflammation and degeneration (including iron accumulation, microglia and astrocyte activation and ectopic lymphoid follicle formation), which will shape our understanding of the disease and are already driving the development of novel therapeutic approaches. In addition, although there is evidence for remyelination in patients, strategies to promote it in patients are mostly lacking, probably due to our incomplete knowledge of its mechanisms.

In this Special Issue, we will try to fill these knowledge gaps, publishing research addressing the molecular mechanisms underlying the different aspects of inflammation, degeneration and repair in multiple sclerosis.

Dr. Joao Jose Cerqueira
Dr. Fernanda Marques
Guest Editors

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Keywords

  • astrocytes
  • axonal transection
  • demyelination
  • EBV
  • immunometabolism
  • insulin signaling
  • iron
  • lymphotoxin
  • microglia
  • mitochondria
  • neurodegeneration
  • oligodendrocytes
  • remyelination
  • brain barriers

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Published Papers (1 paper)

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Review

30 pages, 3185 KiB  
Review
Glial Cells as Key Regulators in Neuroinflammatory Mechanisms Associated with Multiple Sclerosis
by Styliani Theophanous, Irene Sargiannidou and Kleopas A. Kleopa
Int. J. Mol. Sci. 2024, 25(17), 9588; https://doi.org/10.3390/ijms25179588 - 4 Sep 2024
Viewed by 212
Abstract
Even though several highly effective treatments have been developed for multiple sclerosis (MS), the underlying pathological mechanisms and drivers of the disease have not been fully elucidated. In recent years, there has been a growing interest in studying neuroinflammation in the context of [...] Read more.
Even though several highly effective treatments have been developed for multiple sclerosis (MS), the underlying pathological mechanisms and drivers of the disease have not been fully elucidated. In recent years, there has been a growing interest in studying neuroinflammation in the context of glial cell involvement as there is increasing evidence of their central role in disease progression. Although glial cell communication and proper function underlies brain homeostasis and maintenance, their multiple effects in an MS brain remain complex and controversial. In this review, we aim to provide an overview of the contribution of glial cells, oligodendrocytes, astrocytes, and microglia in the pathology of MS during both the activation and orchestration of inflammatory mechanisms, as well as of their synergistic effects during the repair and restoration of function. Additionally, we discuss how the understanding of glial cell involvement in MS may provide new therapeutic targets either to limit disease progression or to facilitate repair. Full article
(This article belongs to the Special Issue Molecular Advances and Perspectives in Multiple Sclerosis)
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