ArticleAging cell2021
Functional genomic analyses highlight a shift in Gpr17-regulated cellular processes in oligodendrocyte progenitor cells and underlying myelin dysregulation in the aged mouse cerebrum.
Article in Aging cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 57 citations in OpenAlex.
- Age-dependent transcriptomic effects of morphine in the frontal cortex of female mice.Neuropharmacology · 2026Article
- Adult leptomeningeal vestigial neural crest-derived multipotent cells promote vascular repair after stroke.Cell reports · 2026Article
- Review
- APOE genotype influences on the brain metabolome of aging mice - role for mitochondrial energetics in mechanisms of resilience in APOE2 genotype.Molecular neurodegeneration · 2025Article
- Glial Cells and Aging: From the CNS to the Cerebellum.International journal of molecular sciences · 2025Review
- Inhibition of GPR17/ID2 Axis Improve Remyelination and Cognitive Recovery after SAH by Mediating OPC Differentiation in Rat Model.Translational stroke research · 2025Article
- Oligodendroglia in Ageing and Age-Dependent Neurodegenerative Diseases.Advances in neurobiology · 2025Review
- Morphology of Oligodendroglial Cells.Advances in neurobiology · 2025Review
- Cellular Components of the Blood-Brain Barrier and Their Involvement in Aging-Associated Cognitive Impairment.Aging and disease · 2024Review
- Sex as a Determinant of Age-Related Changes in the Brain.International journal of molecular sciences · 2024Review
- The Genomic Intersection of Oligodendrocyte Dynamics in Schizophrenia and Aging Unravels Novel Pathological Mechanisms and Therapeutic Potentials.International journal of molecular sciences · 2024Review
- Age-related changes after intracerebral hemorrhage: a comparative proteomics analysis of perihematomal tissue.Experimental biology and medicine (Maywood, N.J.) · 2024Article
- Aging differentially alters the transcriptome and landscape of chromatin accessibility in the male and female mouse hippocampus.Frontiers in molecular neuroscience · 2024Article
- What Are the Roles of Oligodendrocyte Precursor Cells in Normal and Pathologic Conditions?Neurology · 2023Article
- Article
- Trem2 Enhances Demyelination in theBiomedicines · 2023Article
- Novel therapeutic approaches to target neurodegeneration.British journal of pharmacology · 2023Review
- Altered Purinergic Signaling in Neurodevelopmental Disorders: Focus on P2 Receptors.Biomolecules · 2023Review
- Deep Imaging to Dissect Microvascular Contributions to White Matter Degeneration in Rodent Models of Dementia.Stroke · 2023Review
- Next generation drug connectivity mapping for acquiring therapeutic agents to differentially regulate myelination.Neural regeneration research · 2023Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
Abstract
Brain ageing is characterised by a decline in neuronal function and associated cognitive deficits. There is increasing evidence that myelin disruption is an important factor that contributes to the age-related loss of brain plasticity and repair responses. In the brain, myelin is produced by oligodendrocytes, which are generated throughout life by oligodendrocyte progenitor cells (OPCs). Currently, a leading hypothesis points to ageing as a major reason for the ultimate breakdown of remyelination in Multiple Sclerosis (MS). However, an incomplete understanding of the cellular and molecular processes underlying brain ageing hinders the development of regenerative strategies. Here, our combined systems biology and neurobiological approach demonstrate that oligodendroglial and myelin genes are amongst the most altered in the ageing mouse cerebrum. This was underscored by the identification of causal links between signalling pathways and their downstream transcriptional networks that define oligodendroglial disruption in ageing. The results highlighted that the G-protein coupled receptor Gpr17 is central to the disruption of OPCs in ageing and this was confirmed by genetic fate-mapping and cellular analyses. Finally, we used systems biology strategies to identify therapeutic agents that rejuvenate OPCs and restore myelination in age-related neuropathological contexts.
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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.