ArticleNature aging2026
ACSS2 maintains oligodendrocyte progenitor cell pool and is required for myelination during development and aging.
Article in Nature aging, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Myelin Repair as a Neuroprotective Strategy for Multiple Sclerosis: From Bench to Bedside.Medicina (Kaunas, Lithuania) · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
The reduction in number and decreased differentiation capacity of oligodendrocyte progenitor cells (OPCs) directly affect myelination in demyelinating diseases and aging, but the underlying mechanisms remain incompletely characterized. Here we observed a marked decline in the number of OPCs during aging, notably within the subpopulation highly expressing Acss2, which encodes acetyl-CoA synthetase 2 (ACSS2). Deletion of ACSS2 in the oligodendrocyte lineage resulted in a reduced OPC population, defective myelinogenesis during development, impaired myelin maintenance in adulthood and aging, and exacerbated age-related cognitive deficits. Mechanistically, ACSS2-mediated acetylation of H4K12 and H3K27 enhances the expression of Gria2, an AMPA receptor subunit critical for OPC proliferation. Furthermore, supplementation with the ACSS2 substrate acetate preserved the number of OPCs, promoted remyelination after injury and improved cognitive function in aged mice. Together, our findings highlight the essential role of ACSS2-mediated acetate utilization in maintaining the OPC population and promoting myelin production during development, demyelination and aging.
Indexed as
Identifiers
41781676What Socratic 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 Socratic graph.