ArticleJournal of inflammation research2021
Microglia Impede Oligodendrocyte Generation in Aged Brain.
Article in Journal of inflammation research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Genetic Deletion of Adenosine AGlia · 2026Article
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- Coordinated transcriptional shifts in microglia and oligodendrocytes from neurodevelopment to inflammaging.npj aging · 2026Article
- Integrated protocol for concurrent generation of microglial and neuronal cells in human cerebral organoids.BMC methods · 2026Article
- Article
- Making tracks: microglia and the extracellular matrix.Molecular neurodegeneration · 2025Review
- Review
- Interaction of nutritional and inflammatory levels on all-cause mortality among individuals with rheumatoid arthritis: a prospective cohort study.Clinical rheumatology · 2025Article
- The Role of Glial Cell Senescence in Alzheimer's Disease.Journal of neurochemistry · 2025Review
- Should We Consider Neurodegeneration by Itself or in a Triangulation with Neuroinflammation and Demyelination? The Example of Multiple Sclerosis and Beyond.International journal of molecular sciences · 2024Review
- Alzheimer's Disease, Obesity, and Type 2 Diabetes: Focus on Common Neuroglial Dysfunctions (Critical Review and New Data on Human Brain and Models).Brain sciences · 2024Review
- A New Acquaintance of Oligodendrocyte Precursor Cells in the Central Nervous System.Neuroscience bulletin · 2024Review
- Microglia regulation of central nervous system myelin health and regeneration.Nature reviews. Immunology · 2024Review
- Integrating spatial and single-cell transcriptomics data using deep generative models with SpatialScope.Nature communications · 2023Article
- Bystanders or not? Microglia and lymphocytes in aging and stroke.Neural regeneration research · 2023Review
- Aging microglia.Cellular and molecular life sciences : CMLS · 2023Review
- TREM2 mediates physical exercise-promoted neural functional recovery in rats with ischemic stroke via microglia-promoted white matter repair.Journal of neuroinflammation · 2023Article
- Enhancing axonal myelination in seniors: A review exploring the potential impact cannabis has on myelination in the aged brain.Frontiers in aging neuroscience · 2023Review
- Biological agents and the aging brain: glial inflammation and neurotoxic signaling.Frontiers in aging · 2023Review
- Regulatory T Cell Therapeutics for Neuroinflammatory Disorders.Critical reviews in immunology · 2022Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeAge-related increase in myelin loss may be responsible for brain atrophy, and the mechanism is not completely understood. We aim to comprehensively delineate oligodendrocyte heterogeneity in young and aged mice and to reveal the underlying mechanism for myelin loss during aging.
methodsDiffusion tensor imaging and immunofluorescent staining were performed to verify the demyelination in the aged brains of both rodents and human. Further, the single-cell RNA sequencing data of all brain cells from young and aged mice were deeply analyzed to identify the subsets of oligodendrocyte lineage cells. Cell-to-cell interaction analysis was performed to detect the mechanism of observed changes in oligodendrocyte generation.
resultsOligodendrocytes were observed to up-regulate several senescence associated genes in aged brain. Four clusters of oligodendrocyte precursor cells (OPCs) were identified in both young and aged brains. The number of those OPCs in basal state was significantly increased, while the OPCs in the procedure of differentiation were immensely decreased in aged brain. Furthermore, it was identified that activated microglia in the aged brain released inflammatory factors to suppress OPC differentiation. Stat1 might be a potential target to transform senescent microglia into tissue repair type to promote oligodendrocyte generation.
conclusionThese results provided a perspective on how age activated microglia could impede remyelination and might give a new therapeutic target for age-related remyelinating diseases.
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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.