Exploring causal relationships between epigenetic age acceleration and Alzheimer's disease: a bidirectional Mendelian randomization study.

ABSTRACT:

Background

Alzheimer's disease (AD) is identified by a distinct progression of aging-associated cognitive and functional impairment. Recent advances recognize the DNA methylation-based epigenetic clock as a precise predictor of aging processes and their related health outcomes. However, observational studies exploring this link are often compromised by confounding factors and reverse causality bias. To address the question, our study employs a bidirectional Mendelian randomization (MR) analysis to explore the causal relationship between epigenetic age acceleration (EAA) and AD.

Methods

Genome-wide association study (GWAS) statistics for epigenetic clocks (GrimAge, PhenoAge, HorvathAge, and HannumAge) were sourced from Edinburgh DataShare and the Alzheimer Disease Genetics Co

SUBMITTER: Liu H 

PROVIDER: S-EPMC12495807 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature