ArticleGlia2017
Lineage tracing reveals dynamic changes in oligodendrocyte precursor cells following cuprizone-induced demyelination.
Article in Glia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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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Who cites it
61 citing papers in PubMed, 102 citations in OpenAlex.
- Article
- Article
- Myelin is repaired by constitutive differentiation of oligodendrocyte progenitors.Science (New York, N.Y.) · 2026Article
- Acute TREM2 inhibition depletes MAFB-high microglia and hinders remyelination.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Siponimod supports remyelination in the non-supportive environment.Scientific reports · 2025Article
- Plasticity of Myelination.Advances in neurobiology · 2025Review
- Demyelination and Remyelination: General Principles.Advances in neurobiology · 2025Review
- Respiratory infection with influenza A virus delays remyelination and alters oligodendrocyte metabolism.iScience · 2024Article
- Low intensity repetitive transcranial magnetic stimulation enhances remyelination by newborn and surviving oligodendrocytes in the cuprizone model of toxic demyelination.Cellular and molecular life sciences : CMLS · 2024Article
- A molecularly defined subpopulation of oligodendrocyte precursor cells controls the generation of myelinating oligodendrocytes during postnatal development.PLoS biology · 2024Article
- Long-term in vivo three-photon imaging reveals region-specific differences in healthy and regenerative oligodendrogenesis.Nature neuroscience · 2024Article
- Automated analysis of gray matter damage in aged mice reveals impaired remyelination in the cuprizone model.Brain pathology (Zurich, Switzerland) · 2024Article
- How to Use the Cuprizone Model to Study De- and Remyelination.International journal of molecular sciences · 2024Review
- Article
- Long-termbioRxiv : the preprint server for biology · 2023Article
- Insufficient Oligodendrocyte Turnover in Optic Nerve Contributes to Age-Related Axon Loss and Visual Deficits.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Fractalkine enhances oligodendrocyte regeneration and remyelination in a demyelination mouse model.Stem cell reports · 2023Article
- Remyelination in animal models of multiple sclerosis: finding the elusive grail of regeneration.Frontiers in molecular neuroscience · 2023Review
- Contribution of Intravital Neuroimaging to Study Animal Models of Multiple Sclerosis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- Oligodendrocyte precursor cells ingest axons in the mouse neocortex.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
1 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
The regeneration of oligodendrocytes is a crucial step in recovery from demyelination, as surviving oligodendrocytes exhibit limited structural plasticity and rarely form additional myelin sheaths. New oligodendrocytes arise through the differentiation of platelet-derived growth factor receptor α (PDGFRα) expressing oligodendrocyte progenitor cells (OPCs) that are widely distributed throughout the CNS. Although there has been detailed investigation of the behavior of these progenitors in white matter, recent studies suggest that disease burden in multiple sclerosis (MS) is more strongly correlated with gray matter atrophy. The timing and efficiency of remyelination in gray matter is distinct from white matter, but the dynamics of OPCs that contribute to these differences have not been defined. Here, we used in vivo genetic fate tracing to determine the behavior of OPCs in gray and white matter regions in response to cuprizone-induced demyelination. Our studies indicate that the temporal dynamics of OPC differentiation varies significantly between white and gray matter. While OPCs rapidly repopulate the corpus callosum and mature into CC1 expressing mature oligodendrocytes, OPC differentiation in the cingulate cortex and hippocampus occurs much more slowly, resulting in a delay in remyelination relative to the corpus callosum. The protracted maturation of OPCs in gray matter may contribute to greater axonal pathology and disease burden in MS.
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Registered trials
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.