ArticlemedRxiv : the preprint server for health sciences2025
Associations of Epigenetic Age Acceleration with Motor Impairment: Evidence from the PPMI Cohort.
Article in medRxiv : the preprint server for health sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objective: Motor decline is a hallmark of Parkinson's disease (PD) and biological aging. While epigenetic clocks measure systemic biological aging, their specific relationship with neuromotor function in the context of aging and neurodegeneration remains under-characterized. This study utilized data from the Parkinson's Progression Markers Initiative (PPMI) to examine the relationships between multiple DNA methylation-based epigenetic aging measures and motor impairment across distinct domains. Methods: We utilized longitudinal phenotype and whole-blood DNA methylation data from the PPMI cohort. Seven epigenetic aging measures were calculated, including first-generation clocks (Horvath v1, Hannum), risk-optimized second-generation clocks (PhenoAge, GrimAge v1 and v2), a deep-learning estimator (AltumAge), and a pace-of-aging biomarker (DunedinPACE). Motor function was assessed using the MDS-UPDRS, which captures patient-reported disability, global staging (Hoehn & Yahr), and specific motor signs, including tremor, bradykinesia, and postural instability. Cross-sectional associations were evaluated using binary or ordinal logistic regression, while longitudinal repeated measures were analyzed using generalized estimating equations (GEE) and cumulative link mixed models (CLMM), with adjustments for multiple comparisons made using the false discovery rate (FDR). Results: Cross-sectional analyses yielded limited evidence, identifying only a specific association between Horvath v1 acceleration and postural tremor in males ( Conclusions: Accelerated epigenetic aging is robustly associated with the longitudinal progression of tremor impairment in PD, with associations being particularly consistent and multi-dimensional in men. These findings suggest that systemic biological aging, as captured by both first- and second-generation clocks, disproportionately exacerbates tremor circuitry distinct from the dopaminergic pathways that drive bradykinesia. Epigenetic clocks may serve as valuable biomarkers for monitoring progression and risk stratification, particularly for tremor-dominant phenotypes.
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