ArticleFrontiers in cellular neuroscience2022
Age and Alzheimer's Disease-Related Oligodendrocyte Changes in Hippocampal Subregions.
Article in Frontiers in cellular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 30 citations in OpenAlex.
- Does perturbed adaptive myelination contribute to cognitive dysfunction in Alzheimer's disease?PLoS biology · 2026Article
- Emodin Suppresses the RAGE/ROCK1 Pathway to Modulate the Oligodendrocyte Lineage and Ameliorate Demyelination in Vascular Dementia Rats.CNS neuroscience & therapeutics · 2026Article
- Oligodendrocyte precursor cells-microglia crosstalk via BMP4 drives microglial neuroprotective response and mitigates Alzheimer's disease.Signal transduction and targeted therapy · 2026Article
- Induction of neurodegeneration in the hippocampus of senescence-accelerated mouse-prone 8 (SAMP8) mice by blood-brain barrier-crossing serum amyloid P component.Journal of neuroinflammation · 2026Article
- BT-11 targets the LANCL2 pathway to attenuate cognitive deficits and hippocampal pathology in Alzheimer's transgenic rats.Scientific reports · 2025Article
- Article
- 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
- Article
- Stimulating myelin restoration with BDNF: a promising therapeutic approach for Alzheimer's disease.Frontiers in cellular neuroscience · 2024Review
- Secondary Central Nervous System Demyelinating Disorders in the Elderly: A Narrative Review.Healthcare (Basel, Switzerland) · 2023Review
- Myelin in Alzheimer's disease: culprit or bystander?Acta neuropathologica communications · 2023Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Oligodendrocytes (OLs) form myelin sheaths and provide metabolic support to axons in the CNS. Although most OLs develop during early postnatal life, OL generation continues in adulthood, and this late oligodendrogenesis may contribute to neuronal network plasticity in the adult brain. We used genetic tools for OL labeling and fate tracing of OL progenitors (OPCs), thereby determining OL population growth in hippocampal subregions with normal aging. OL numbers increased up to at least 1 year of age, but the rates and degrees of this OL change differed among hippocampal subregions. In particular, adult oligodendrogenesis was most prominent in the CA3 and CA4 subregions. In Alzheimer's disease-like conditions, OL loss was also most severe in the CA3 and CA4 of APP/PS1 mice, although the disease did not impair the rate of OPC differentiation into OLs in those regions. Such region-specific, dynamic OL changes were not correlated with those of OPCs or astrocytes, or the regional distribution of Aβ deposits. Our findings suggest subregion-dependent mechanisms for myelin plasticity and disease-associated OL vulnerability in the adult hippocampus.
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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.