ArticleFrontiers in cellular neuroscience2025
Thinning of originally-existing, mature myelin represents a nondestructive form of myelin loss in the adult CNS.
Article in Frontiers in cellular neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Oligodendrocytes Are Active Participants in the Pathogenesis of Multiple Sclerosis and Its Animal Models.International journal of molecular sciences · 2026Review
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Authors and funding
2 authors.
Funding
Abstract
The main function of oligodendrocytes is to assemble and maintain myelin that wraps and insulates axons in the central nervous system (CNS). Traditionally, myelin structure, particularly its thickness, was believed to remain remarkably stable in adulthood (including early and middle adulthood, but not late adulthood or aging). However, emerging evidence reveals that the thickness of originally-existing, mature myelin (OEM) can undergo dynamic changes in the adult CNS. This overview highlights recent findings on the alteration of OEM thickness in the adult CNS, explores the underlying mechanisms, and proposes that progressive thinning of OEM represents a novel, nondestructive form of myelin loss in myelin disorders of the CNS.
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Registered trials
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