Increased stress in early life epigenetically rewires pathways related to aging and longevity
- 1University of Edinburgh
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.
Related
- Divergent Retrograde Signaling Pathways Coordinate Longevity and Metformin Responses in Complex I and Complex IV Deficient C. elegans
- Fatigue-related changes in value-based decision-making during listening are associated with increased frontal cortical activation
- RNA-sequencing of butyrate-treated human lymphoblastoid cell lines shows dysregulated genes of multiple disease-related pathways
- Human factor H-related protein 5 modulates the classical and lectin complement pathways on selected host ligands
- Enniatin B attenuates deoxynivalenol-induced toxicity in liver cells and modulates lipid metabolism-related pathways
BibTeX
@misc{olova2026increased,
title = {{Increased stress in early life epigenetically rewires pathways related to aging and longevity}},
author = {N. N. Olova and T. Zhou and W. Boner and R. Gillespie and E. R. Ivimey-Cook and R. Marioni and E. J. A. Cunningham and T. Chandra and T. J. Little and P. Monaghan and D. M. Dominoni},
howpublished = {bioRxiv},
year = {2026},
month = sep,
doi = {10.64898/2026.09.30.755600},
url = {https://www.biorxiv.org/content/10.64898/2026.09.30.755600v1},
note = {CC BY-NC-ND},
}
RIS
TY - UNPB
TI - Increased stress in early life epigenetically rewires pathways related to aging and longevity
AU - N. N. Olova
AU - T. Zhou
AU - W. Boner
AU - R. Gillespie
AU - E. R. Ivimey-Cook
AU - R. Marioni
AU - E. J. A. Cunningham
AU - T. Chandra
AU - T. J. Little
AU - P. Monaghan
AU - D. M. Dominoni
PY - 2026
DA - 2026/09/30
PB - bioRxiv
DO - 10.64898/2026.09.30.755600
UR - https://www.biorxiv.org/content/10.64898/2026.09.30.755600v1
AB - 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.
ER -