ArticleProceedings of the National Academy of Sciences of the United States of America2017
Thin myelin sheaths as the hallmark of remyelination persist over time and preserve axon function.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed.
- Article
- Review
- Repeated ablations of mature Tmem10Cell death & disease · 2025Article
- Neurological disability and brain grey matter atrophy in primary progressive multiple sclerosis are determined by microstructural lesional changes, but not by lesion load.Journal of neurology · 2025Article
- Demyelination and Remyelination: General Principles.Advances in neurobiology · 2025Review
- Thinning of originally-existing, mature myelin represents a nondestructive form of myelin loss in the adult CNS.Frontiers in cellular neuroscience · 2025Article
- Trem2-deficiency aggravates and accelerates age-related myelin degeneration.Acta neuropathologica communications · 2024Article
- Article
- N-Acetylaspartate Drives Oligodendroglial Differentiation via Histone Deacetylase Activation.Cells · 2023Article
- Article
- Mechanisms of Demyelination and Remyelination Strategies for Multiple Sclerosis.International journal of molecular sciences · 2023Review
- Remyelination in Multiple Sclerosis: Findings in the Cuprizone Model.International journal of molecular sciences · 2022Review
- CNS myelination requires VAMP2/3-mediated membrane expansion in oligodendrocytes.Nature communications · 2022Article
- The landscape of targets and lead molecules for remyelination.Nature chemical biology · 2022Review
- White matter tract conductivity is resistant to wide variations in paranodal structure and myelin thickness accompanying the loss of Tyro3: an experimental and simulated analysis.Brain structure & function · 2022Article
- Lumbar spine intrathecal transplantation of neural precursor cells promotes oligodendrocyte proliferation in hot spots of chronic demyelination.Brain pathology (Zurich, Switzerland) · 2022Article
- Acute axon damage and demyelination are mitigated by 4-aminopyridine (4-AP) therapy after experimental traumatic brain injury.Acta neuropathologica communications · 2022Article
- Restoration of spinal cord injury: From endogenous repairing process to cellular therapy.Frontiers in cellular neuroscience · 2022Review
- Myelin water imaging depends on white matter fiber orientation in the human brain.Magnetic resonance in medicine · 2021Article
- Prolonging the integrated stress response enhances CNS remyelination in an inflammatory environment.eLife · 2021Article
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4 authors.
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Abstract
The presence of thin myelin sheaths in the adult CNS is recognized as a marker of remyelination, although the reason there is not a recovery from demyelination to normal myelin sheath thickness remains unknown. Remyelination is the default pathway after myelin loss in all mammalian species, in both naturally occurring and experimental disease. However, there remains uncertainty about whether these thin sheaths thicken with time and whether they remain viable for extended periods. We provide two lines of evidence here that thin myelin sheaths may persist indefinitely in long-lived animal models. In the first, we have followed thin myelin sheaths in a model of delayed myelination during a period of 13 years that we propose results in the same myelin sheath deficiencies as seen in remyelination; that is, thin myelin sheaths and short internodes. We show that the myelin sheaths remain thin and stable on many axons throughout this period with no detrimental effects on axons. In a second model system, in which there is widespread demyelination of the spinal cord and optic nerves, we also show that thinly remyelinated axons with short internodes persist for over the course of 2 y. These studies confirm the persistence and longevity of thin myelin sheaths and the importance of remyelination to the long-term health and function of the CNS.
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