Increased stress in early life epigenetically rewires pathways related to aging and longevity
Abstract
Environmental conditions experienced early in life have profound consequences for vertebrate health, yet the molecular pathways linking developmental stress to aging and reduced lifespan remain poorly understood. Through a novel highly accurate epigenetic clock, developed from RRBS-based blood DNA methylation profiles, we show that experimental lifespan-reducing early-life stress rapidly accelerates epigenetic age in zebra finch chicks (Taeniopygia guttata). Corticosterone-treated 29-day-old chicks share differentially methylated loci with non-treated aged birds and cluster with 6-month-old birds. The transcriptional repressor ZBTB16 emerges as an epigenetically top age-correlated gene and is strongest affected by corticosterone. Elevated developmental corticosterone causes rapid epigenetic remodelling of metabolic pathways well-established in aging and longevity. Our results demonstrate epigenetic rewiring of the aging trajectory through conserved stress-survival mechanisms immediately following elevated early-life stress exposure.
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Research summary
Early-life stress exposure epigenetically rewires metabolic pathways associated with aging, accelerating biological age in zebra finches. This study provides mechanistic insight into how developmental stressors influence the aging trajectory via conserved epigenetic mechanisms, contributing to the understanding of the root causes of accelerated aging rather than just treating symptoms.
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