ArticleFrontiers in cellular neuroscience2020
Accelerated Dystrophy and Decay of Oligodendrocyte Precursor Cells in the APP/PS1 Model of Alzheimer's-Like Pathology.
Article in Frontiers in cellular neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed.
- Deletion ofBiology · 2026Article
- Dysregulated oligodendrocyte and myelin dynamics as an early pathological feature of neuropil degeneration in Alzheimer's disease: an ultrastructural study.Acta neuropathologica communications · 2026Article
- Extracellular Vesicles in Alzheimer's Disease: Mechanisms, Biomarkers, and Therapeutic Engineering.International journal of molecular sciences · 2026Review
- Emerging Role of Oligodendrocytes Malfunction in the Progression of Alzheimer's Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Review
- Critical analysis of translational potential of rodent models of white matter pathology across a wide spectrum of human diseases.Cell death & disease · 2025Review
- Roles of Ion Channels in Oligodendrocyte Precursor Cells: From Physiology to Pathology.International journal of molecular sciences · 2025Review
- Article
- The Many Lives of an Oligodendrocyte Precursor Cell.Annual review of neuroscience · 2025Review
- A single-cell transcriptomic atlas of all cell types in the brain of 5xFAD Alzheimer mice in response to dietary inulin supplementation.BMC biology · 2025Article
- Human longevity and Alzheimer's disease variants act via microglia and oligodendrocyte gene networks.Brain : a journal of neurology · 2025Article
- A neurodegenerative cellular stress response linked to dark microglia and toxic lipid secretion.Neuron · 2025Article
- APOEε4 alters ApoE and Fabp7 in frontal cortex white matter in prodromal Alzheimer's disease.Journal of neuroinflammation · 2025Article
- Integrated multimodal cell atlas of Alzheimer's disease.Nature neuroscience · 2024Article
- All GLP-1 Agonists Should, Theoretically, Cure Alzheimer's Dementia but Dulaglutide Might Be More Effective Than the Others.Journal of clinical medicine · 2024Review
- Mitochondrial calcium signaling in non-neuronal cells: Implications for Alzheimer's disease pathogenesis.Biochimica et biophysica acta. Molecular basis of disease · 2024Review
- Recognizing Alzheimer's disease from perspective of oligodendrocytes: Phenomena or pathogenesis?CNS neuroscience & therapeutics · 2024Review
- Stimulating myelin restoration with BDNF: a promising therapeutic approach for Alzheimer's disease.Frontiers in cellular neuroscience · 2024Review
- Oligodendrocyte progenitor cells in Alzheimer's disease: from physiology to pathology.Translational neurodegeneration · 2023Review
- The role of glial autophagy in Alzheimer's disease.Molecular psychiatry · 2023Review
- Emerging roles of oligodendrocyte precursor cells in neural circuit development and remodeling.Trends in neurosciences · 2023Review
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7 authors.
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Abstract
Myelin disruption is a feature of natural aging and Alzheimer's disease (AD). In the CNS, myelin is produced by oligodendrocytes, which are generated throughout life by oligodendrocyte progenitor cells (OPCs). Here, we examined age-related changes in OPCs in APP/PS1 mice, a model for AD-like pathology, compared with non-transgenic (Tg) age-matched controls. The analysis was performed in the CA1 area of the hippocampus following immunolabeling for NG2 with the nuclear dye Hoescht, to identify OPC and OPC sister cells, a measure of OPC replication. The results indicate a significant decrease in the number of OPCs at 9 months in APP/PS1 mice, compared to age-matched controls, without further decline at 14 months. Also, the number of OPC sister cells declined significantly at 14 months in APP/PS1 mice, which was not observed in age-matched controls. Notably, OPCs also displayed marked morphological changes at 14 months in APP/PS1 mice, characterized by an overall shrinkage of OPC process domains and increased process branching. The results indicate that OPC disruption is a pathological sign in the APP/PS1 mouse model of AD.
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