ArticleCureus2026
Focal Polycomb-Mediated Repression of Neuronal Identity and Synaptic Maintenance Genes in Aging Neurons.
Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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.
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Who cites it
3 citing papers in PubMed.
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1 author.
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Abstract
backgroundNeuronal aging is accompanied by changes in chromatin regulation, but the gene-level mechanisms that connect epigenetic remodeling to circuit decline remain incompletely defined.
methodsWe performed a secondary, Activity-by-Contact (ABC)-inspired analysis of histone H3 lysine 27 trimethylation (H3K27me3) signal tracks from purified mouse forebrain neurons in GSE190102, focusing on the contrast between young adult neurons at 3 months and old neurons at 24 months, with 12-month samples used to evaluate age trajectories.
resultsWe identified 1,500 age-associated region-gene assignments, with a strong predominance of H3K27me3 gain. In total, 1,383 assignments, representing 92% of the interpreted set, showed gain, whereas 117, representing 8%, showed loss. The strongest gain module involved clustered protocadherin genes, including multiple Pcdhb genes, Pcdhgb4, Pcdhgc3, and Pcdha7. A second gain module involved synaptic maintenance and neurotransmission genes, including Nlgn3, Cask, Dlg4, Dlg3, Syn1, Chrm2, Chrna5, and Chrnb4. These changes were accompanied by a smaller loss module involving chromatin, transcriptional, lysosomal, and stress-response candidates, including Med14, Med12, Atp6ap2, and Heph. Functional enrichment highlighted calcium-dependent cell-cell adhesion, cell-adhesion molecules, neuroactive ligand-receptor interaction, and cholinergic synapse pathways.
conclusionsThese results support a working model in which aging neurons undergo Polycomb redistribution rather than simple uniform loss of H3K27me3. In this model, focal hyper-repression of neuronal identity and synaptic scaffold programs may reduce circuit precision, while selected loss of repression at stress and transcriptional regulators may permit compensatory or maladaptive rewiring. We propose a compact candidate 14-gene Synaptic Epigenetic Aging Signature as a practical biomarker and screening panel for cognitive aging, neuromodulatory treatment stratification, and future locus-specific epigenome-editing studies.
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