ArticleBrain and behavior2020
Vitamin D increases remyelination by promoting oligodendrocyte lineage differentiation.
Article in Brain and behavior, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 3 of them syntheses that pooled it.
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Who cites it
36 citing papers in PubMed, 3 syntheses or guidelines pooled it, 59 citations in OpenAlex.
- Impact of vitamin D on the prognosis after spinal cord injury: A systematic review.Frontiers in nutrition · 2023Pooled it
- Vitamin D and schizophrenia: 20 years on.Molecular psychiatry · 2021Pooled it
- Low circulating 25-hydroxyvitamin D level is associated with increased colorectal cancer mortality: a systematic review and dose-response meta-analysis.Bioscience reports · 2020Pooled it
- Shedding Light on Interaction Between Neurological Symptoms and Psychiatric Episodes in Multiple Sclerosis: Novel Hypothesis and Therapeutic Avenues.Molecular neurobiology · 2026Review
- Vitamin D Signaling in Neurodegenerative Disorders: Mechanisms, Therapeutic Potential, and Clinical Implications.Nutrients · 2026Review
- The Role of Vitamin D in Neuropathic Pain: Biological Mechanisms and Clinical Relevance.International journal of molecular sciences · 2026Review
- Review
- Pharmacological Therapies for Consequences of Perinatal Hypoxic-Ischemic Brain Injury: Where Are We Now?International journal of molecular sciences · 2025Review
- Vitamin D Deficiency Does Not Affect Cognition and Neurogenesis in Adult C57Bl/6 Mice.Nutrients · 2024Article
- Guggulsterone Selectively Modulates STAT-3, mTOR, and PPAR-Gamma Signaling in a Methylmercury-Exposed Experimental Neurotoxicity: Evidence from CSF, Blood Plasma, and Brain Samples.Molecular neurobiology · 2024Article
- CDP-choline to promote remyelination in multiple sclerosis: the need for a clinical trial.Neural regeneration research · 2023Review
- Review
- In Vitro Effects of Methylprednisolone over Oligodendroglial Cells: Foresight to Future Cell Therapies.Cells · 2023Article
- Radiological Benefits of Vitamin D Status and Supplementation in Patients with MS-A Two-Year Prospective Observational Cohort Study.Nutrients · 2023Observational
- COVID-19 and Multiple Sclerosis: A Complex Relationship Possibly Aggravated by Low Vitamin D Levels.Cells · 2023Review
- Vitamin D Supplementation Practices among Multiple Sclerosis Patients and Professionals.Journal of clinical medicine · 2022Article
- Is there a window of opportunity for the therapeutic use of vitamin D in multiple sclerosis?Neural regeneration research · 2022Review
- Role of Neural Stem Cells and Vitamin D Receptor (VDR)-Mediated Cellular Signaling in the Mitigation of Neurological Diseases.Molecular neurobiology · 2022Review
- Nuclear hormone receptors in demyelinating diseases.Journal of neuroendocrinology · 2022Review
- Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionSeveral experimental studies have suggested the potential remyelinating effects of vitamin D (VitD) supplements regardless of the presence of VitD deficiency. This study aims to analyze neurogenesis in a model of toxic demyelination in order to evaluate the effects of VitD on demyelination and remyelination. MATERIAL AND
methodsWe used 24 male Wistar rats that had received surgical lesions to the corpus callosum and were injected with lysolecithin. Rats were divided into three groups: Group 1 included eight rats with lesions to the corpus callosum but not lysolecithin injections (sham group), group 2 included eight rats with lesions to the corpus callosum that were injected with lysolecithin (lysolecithin group), and group 3 included eight rats with lesions that were injected with lysolecithin and received VitD (VitD group). We analyzed neurogenesis both in the subventricular zone and at the lesion site.
resultsAdministration of VitD promotes the proliferation and differentiation of neural stem cells in the subventricular zone and the migration of these cells to the lesion site in the corpus callosum; these cells subsequently differentiate into oligodendrocyte lineage cells and produce myelin basic protein. This phenomenon was not caused by microglial activation, which was less marked in rats receiving VitD. Megalin expression did not increase at the lesion site, which suggests that VitD is internalized by other mechanisms.
conclusionOur results support the hypothesis that regardless of the presence of VitD deficiency, treatment with VitD may contribute to remyelination by promoting the proliferation of oligodendrocyte precursor cells.
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