ArticleJournal of neuroinflammation2023
Teriflunomide as a therapeutic means for myelin repair.
Article in Journal of neuroinflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Teriflunomide Attenuates Demyelination and Enhances Remyelination in Organotypic Brain Slice Cultures Through Modulation of Glial Cell Dynamics.CNS neuroscience & therapeutics · 2026Article
- Progression-related outcomes of teriflunomide in multiple sclerosis clinical trials.Frontiers in neurology · 2026Review
- Distal median nerve dysfunction and carpal tunnel syndrome in people with multiple sclerosis treated with teriflunomide: an electrodiagnostic study.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Article
- Positive allosteric modulation of AMPA receptors via PF4778574 leads to reduced demyelination and clinical disability in experimental models of multiple sclerosis.Frontiers in immunology · 2025Article
- NOTCH2NLC GGC intermediate repeat with serine induces hypermyelination and early Parkinson's disease-like phenotypes in mice.Molecular neurodegeneration · 2024Article
- Multiple sclerosis drug repurposing for neuroregeneration.Neural regeneration research · 2024Article
- Transgenic expression of the HERV-W envelope protein leads to polarized glial cell populations and a neurodegenerative environment.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Sex differences in the neuronal transcriptome and synaptic mitochondrial function in the cerebral cortex of a multiple sclerosis model.Frontiers in neurology · 2023Article
- Polysialic acid promotes remyelination in cerebellar slice cultures by Siglec-E-dependent modulation of microglia polarization.Frontiers in cellular neuroscience · 2023Article
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Authors and funding
13 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPromotion of myelin repair in the context of demyelinating diseases such as multiple sclerosis (MS) still represents a clinical unmet need, given that this disease is not only characterized by autoimmune activities but also by impaired regeneration processes. Hence, this relates to replacement of lost oligodendrocytes and myelin sheaths-the primary targets of autoimmune attacks. Endogenous remyelination is mainly mediated via activation and differentiation of resident oligodendroglial precursor cells (OPCs), whereas its efficiency remains limited and declines with disease progression and aging. Teriflunomide has been approved as a first-line treatment for relapsing remitting MS. Beyond its role in acting via inhibition of de novo pyrimidine synthesis leading to a cytostatic effect on proliferating lymphocyte subsets, this study aims to uncover its potential to foster myelin repair.
methodsWithin the cuprizone mediated de-/remyelination model teriflunomide dependent effects on oligodendroglial homeostasis and maturation, related to cellular processes important for myelin repair were analyzed in vivo. Teriflunomide administration was performed either as pulse or continuously and markers specific for oligodendroglial maturation and mitochondrial integrity were examined by means of gene expression and immunohistochemical analyses. In addition, axon myelination was determined using electron microscopy.
resultsBoth pulse and constant teriflunomide treatment efficiently boosted myelin repair activities in this model, leading to accelerated generation of oligodendrocytes and restoration of myelin sheaths. Moreover, teriflunomide restored mitochondrial integrity within oligodendroglial cells.
conclusionsThe link between de novo pyrimidine synthesis inhibition, oligodendroglial rescue, and maintenance of mitochondrial homeostasis appears as a key for successful myelin repair and hence for protection of axons from degeneration.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.