Abstract

Relations of DNA methylation markers to other biological aging markers and to psychosocial, behavioral, and health measures remain unclear. The sample included 23 participants (n = 11 cases with psychiatric diagnoses and n = 12 controls without current or lifetime psychiatric disorder), balanced by age and sex. Genomic DNA was extracted from blood samples; the following were performed: genome-wide DNA methylation assay using Illumina 850k methylationEPIC; PCR assays for relative telomere length (RTL) and mitochondrial DNA copy number (mtCN). Exposures were: case status; depression and anxiety symptoms; psychosocial support; subjective and objective cognition. Outcomes were: DNA methylation age (DNAm age); RTL; mtCN; extrinsic and intrinsic epigenetic age acceleration (EEAA and IEAA). Stronger correlation with chronological age was observed for DNAm age (ρ = 0.86; p < 0.0001) compared to RTL (ρ = −0.53; p < 0.01); mtCN was not correlated with age. DNAm age was more strongly correlated with behavioral and health variables than RTL or mtCN; e.g., correlations with DNAm age: body mass index (ρ = 0.36; p = 0.10); smoking pack-years (ρ = 0.37; p = 0.08); physical activity (ρ = −0.56; p = 0.01); alcohol intake (ρ = 0.56; p = 0.01). DNAm age was inversely correlated with psychosocial support (ρ = −0.42; p = 0.048) and Modified Mini-Mental State score (ρ = −0.44; p = 0.01). Anxiety, psychosocial support, and objective cognition were significantly related to accelerated aging; depression and subjective cognition were not. In conclusion, DNAm age correlated more strongly with chronological age and key psychosocial, behavioral, and health variables than RTL or mtCN. Signals for associations with epigenetic aging were observed for psychosocial and neurobehavioral variables.

Highlights

  • Knowledge gaps exist regarding the biological mechanisms that are involved in trajectories of health and aging

  • We examined the correlations between the aging markers (i.e., DNAm age, relative telomere length (RTL), mitochondrial DNA copy number (mtCN), AgeAccel, epigenetic age acceleration (EEAA), and intrinsic epigenetic age acceleration (IEAA)) with the psychosocial and neurobehavioral outcomes of Patient Health Questionnaire-9 (PHQ-9), Generalized Anxiety Disorder-7 (GAD-7), Duke Social Support Index (DSSI) score, 3MS score, delayed recall z-score and STIDA score

  • While only nominally significant at p < 0.05, there was preliminary indication of differential methylation of genes involved in GTPase activity (GO ID:0090630) and cell-cell adhesion (GO ID:0098609) (See Supplementary material). In this pilot study, we observed that chronological age was strongly correlated with DNAm age, and moderately correlated with telomere length, but not correlated with mtCN

Read more

Summary

Introduction

Knowledge gaps exist regarding the biological mechanisms that are involved in trajectories of health and aging. DNA methylation—the addition of a methyl group to the CpG dinucleotide—is an epigenetic mechanism involved in switching genes on and off (gene expression), with the potential to offer critical insights regarding mechanisms of stress, behavior, and aging. DNA methylation markers may enrich the current complement of biological aging markers, such as telomere length and mitochondrial DNA copy number (mtCN)—. Both of which have previously been associated with aging and/or diseases of aging[1,2]. Epigenetic changes may reflect influences of psychosocial, behavioral, and health risk factors relevant to aging and have been implicated in psychiatric disorders[3]. Horvath and co-workers identified and validated a group of 353 CpG markers for evaluating

Methods
Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call