ArticleGeroScience2023
Aging compromises oligodendrocyte precursor cell maturation and efficient remyelination in the monkey brain.
Article in GeroScience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
- Differential effects of environmental enrichment and physical exercise on glial biology in aging and aging-related conditions: a systematic review.Frontiers in cellular neuroscience · 2026Pooled it
- Rethinking the Oligodendrocyte Progenitor Cell: One Cell, Many Functions.The European journal of neuroscience · 2026Review
- Targeting the FOXO4-p53 axis by retro-inverso peptide senolytic agents: a pharmacological strategy to mitigate brain aging and cognitive decline.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Plasma proteomic signatures of cellular aging predict human disease.Nature medicine · 2026Article
- Uncovering Spatiotemporal and Functional Dynamics of Long Non-coding RNAs During Alzheimer's Progression in the Human Brain at Single-Cell Resolution.Molecular neurobiology · 2026Article
- Tissue-specific mutation of pink-1 jointly induces intestinal dysfunction and contributes to dopaminergic neuron degeneration.NPJ Parkinson's disease · 2026Article
- Article
- ACSS2 maintains oligodendrocyte progenitor cell pool and is required for myelination during development and aging.Nature aging · 2026Article
- ACSS2 is essential for myelination via maintenance of the OPC population.Nature aging · 2026Article
- T cell-microglial interactions that impair myelin maintenance and regeneration: cellular mechanisms on white-matter associated changes.Frontiers in immunology · 2026Review
- From Neuron-Centric to Glia-Centric: How Aging Glial Networks Drive Neurodegenerative Disease.Journal of neurochemistry · 2026Review
- Axon collateralization and focal myelin dystrophy alter action potential propagation in multicompartment pyramidal neuron models.PLoS computational biology · 2025Article
- Article
- Interplay Between Aging and Glial Cell Dysfunction: Implications for CNS Health.Life (Basel, Switzerland) · 2025Review
- Aging diminishes interlaminar functional connectivity in the mouse cortical V1 and CA1 hippocampal regions.bioRxiv : the preprint server for biology · 2025Article
- Review
- Spinal Cord Injury and Ageing: The Role of Chronic Neuroinflammation.Aging and disease · 2025Review
- Myelin dysfunction in aging and brain disorders: mechanisms and therapeutic opportunities.Molecular neurodegeneration · 2025Review
- White matter lipid alterations during aging in the rhesus monkey brain.GeroScience · 2025Article
- Are Oligodendrocytes the Culprits or Victims in Alzheimer's Disease.Physiological research · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Age-associated cognitive decline is common among otherwise healthy elderly people, even in the absence of Alzheimer's disease and neuron loss. Instead, white matter loss and myelin damage are strongly associated with cognitive decline. Myelin is subject to lifelong oxidative stress that damages the myelin sheath, which is repaired by cells of the oligodendrocyte lineage. This process is mediated by oligodendrocyte precursor cells (OPCs) that sense the damage and respond by proliferating locally and migrating to the region, where they differentiate into mature myelinating oligodendrocytes. In aging, extensive myelin damage, in combination with inefficient remyelination, leads to chronically damaged myelin and loss of efficient neuronal conduction. This study used the rhesus monkey model of normal aging to examine how myelin regeneration capacity is affected by age. Results show that older subjects have reduced numbers of new BCAS1 + myelinating oligodendrocytes, which are newly formed cells, and that this reduction is associated with poorer cognitive performance. Interestingly, this does not result from limited proliferation of progenitor OPCs. Instead, the transcription factor NKX2.2, which regulates OPCs differentiation, is significantly decreased in aged OPCs. This suggests that these OPCs have a diminished potential for differentiation into mature oligodendrocytes. In addition, mature oligodendrocytes have reduced RNA expression of two essential myelin protein markers, MBP and PLP. These data collectively suggest that in the normal aging brain, there is a reduction in regenerative OPCs as well as myelin production that impairs the capacity for remyelination.
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What OpenQuestion holds
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.