Remyelination: From Basic Science to Therapies

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Nervous System".

Deadline for manuscript submissions: 31 March 2025 | Viewed by 967

Special Issue Editor


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Guest Editor
Department of Biology, University of ‘Tor Vergata’ Rome, Viale Della Ricerca Scientifica, 00133 Rome, Italy
Interests: oligodendroglia differentiation; remyelination; multiple sclerosis; neurodegeneration; intracellular traffic; yeast
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Special Issue Information

Dear Colleagues,

Myelin sheath damage can occur because of autoimmune attacks, inflammatory processes, and viral infections, invariably leading to neurodegeneration. Remyelination is a spontaneous process that can restore cognitive and functional deficits resulting from myelin sheath injury. Myelin regeneration is also neuroprotective; therefore, identifying regenerative therapies will improve patient quality of life by restoring lost functions and reducing disease progression. Despite significant advances in identifying the factors that trigger myelin damage and the mechanisms through which myelin sheath restoration occurs, in both healthy and pathological conditions, effective disease-modifying therapies that halt or reverse myelin degeneration remain an urgent need.

Undoubtedly, the complexity of the pathogenic mechanisms behind demyelination in Multiple Sclerosis (MS), Alzheimer’s Disease (AD), Parkinson’s Disease (PD), and autism spectrum disorders (ASD) makes phenotypic screening and regenerative therapy testing challenging. To decipher this complex scenario, it is essential to consider that remyelination failure is not only due to defects in oligodendrocyte precursor differentiation but is also strongly influenced by alterations in the surrounding environment. Inflammation and aberrant crosstalk between neural and glial cells are among the causes leading to the disruption of homeostatic mechanisms that regulate regenerative processes in the Central Nervous System (CNS). Dysregulation of immunological surveillance of the CNS, exemplified by aberrant microglial activation, and disruption of myelin sheath integrity represent key events in the early stages of various neurodegenerative conditions.

In this Special Issue, we aim to collect manuscripts that shed new light on the cellular events underlying demyelination in MS, PD, AD, and ASD, as well as studies that review the use iPSC-derived cells, organoids, artificial intelligence, and ultrasound technologies to provide new perspectives on the therapeutic potential of regenerative therapies.

Dr. Antonella Ragnini-Wilson
Guest Editor

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Keywords

  • myelin disease
  • neurodegeneration
  • CNS therapy
  • stem cells
  • regenerative therapies

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Published Papers (1 paper)

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Review

29 pages, 810 KiB  
Review
Remyelinating Drugs at a Crossroad: How to Improve Clinical Efficacy and Drug Screenings
by Aland Ibrahim Ahmed Al Jaf, Simone Peria, Tommaso Fabiano and Antonella Ragnini-Wilson
Cells 2024, 13(16), 1326; https://doi.org/10.3390/cells13161326 - 8 Aug 2024
Viewed by 854
Abstract
Axons wrapped around the myelin sheath enable fast transmission of neuronal signals in the Central Nervous System (CNS). Unfortunately, myelin can be damaged by injury, viral infection, and inflammatory and neurodegenerative diseases. Remyelination is a spontaneous process that can restore nerve conductivity and [...] Read more.
Axons wrapped around the myelin sheath enable fast transmission of neuronal signals in the Central Nervous System (CNS). Unfortunately, myelin can be damaged by injury, viral infection, and inflammatory and neurodegenerative diseases. Remyelination is a spontaneous process that can restore nerve conductivity and thus movement and cognition after a demyelination event. Cumulative evidence indicates that remyelination can be pharmacologically stimulated, either by targeting natural inhibitors of Oligodendrocyte Precursor Cells (OPCs) differentiation or by reactivating quiescent Neural Stem Cells (qNSCs) proliferation and differentiation in myelinating Oligodendrocytes (OLs). Although promising results were obtained in animal models for demyelination diseases, none of the compounds identified have passed all the clinical stages. The significant number of patients who could benefit from remyelination therapies reinforces the urgent need to reassess drug selection approaches and develop strategies that effectively promote remyelination. Integrating Artificial Intelligence (AI)-driven technologies with patient-derived cell-based assays and organoid models is expected to lead to novel strategies and drug screening pipelines to achieve this goal. In this review, we explore the current literature on these technologies and their potential to enhance the identification of more effective drugs for clinical use in CNS remyelination therapies. Full article
(This article belongs to the Special Issue Remyelination: From Basic Science to Therapies)
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