Epigenetic aging in Alzheimer's disease: Relation to proteome.

Authors

Bo-Hyun Kim, Hyunwoo Lee, JunPyo Kim, Sang Won Seo, Kwangsik Nho, Alzheimer's Disease Neuroimaging Initiative

Published in

Alzheimer's & dementia : the journal of the Alzheimer's Association. Volume 22. Issue 8. Pages e71732.

Abstract

Alzheimer's disease (AD) arises from heterogeneous biological processes, and long-term environmental exposures may become biologically embedded, as reflected in epigenetic clocks.
We calculated blood DNA methylation-based epigenetic clocks and constructed protein co-abundance networks of cerebrospinal fluid (CSF) proteomics data. We performed association analysis of epigenetic age acceleration with network modules, followed by functional and cell-type enrichment analyses, association analyses of hub proteins with AD endophenotypes, and pseudotime trajectory analysis.
Six network modules were significantly associated with epigenetic age acceleration and were enriched in pathways related to neuronal connectivity, proteostasis, immune activation and remodeling, immune signaling, and immunoepigenetic regulation. Hub proteins demonstrated significant associations with baseline amyloid/tau/neurodegeneration biomarkers and longitudinal cognitive changes. Pseudotime analysis revealed continuous, non-linear variation in epigenetic age acceleration along the inferred trajectory.
Our CSF proteomics study identified neuronal, proteostatic, and immune-related molecular signatures associated with epigenetic age acceleration in AD.

PMID:
42554263
Bibliographic data and abstract were imported from PubMed on 05 Aug 2026.

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