Authors
Baptiste Sadoughi, Rachel M Petersen, Sam K Patterson, Elizabeth Slikas, Christine Adjangba, Nicholas Ryan, Christina E Costa, Laura E Newman, Marina M Watowich, Cameron R Kelsey, Ashlee Greenier, Elisabeth A Goldman, Josué E Negrón-Del Valle, Daniel Phillips, Indya Thompson, Samuel E Bauman Surratt, Olga González, Nicole Compo, Armando Burgos, Cayo Biobank Research Unit‡, Alex R DeCasien, Kenneth L Chiou, Christopher S Walker, Angelina V Ruiz Lambides, Melween I Martínez, Kirstin N Sterner, Amanda D Melin, Lauren J N Brent, James P Higham, Michael J Montague, Michael L Platt, Noah Snyder-Mackler, Amanda J Lea, Susan C Antón, Lauren J N Brent, James P Higham, Melween I Martínez, Amanda D Melin, Michael J Montague, Michael L Platt, Jerome Sallet, Noah Snyder-Mackler, Cayo Biobank Research Unit
Published in
Science (New York, N.Y.). Volume 392. Issue 6804. Pages eaea4922. Jun 18, 2026. Epub Jun 18, 2026.
Abstract
Age and early life adversity (ELA) are key determinants of health, but whether they affect similar physiological mechanisms across tissues is unknown. We generated DNA methylation (DNAm) profiles across 14 tissues in 237 semi-free-ranging rhesus macaques with naturally occurring ELA. Age-associated DNAm was predominantly tissue dependent, yet tissue-specific epigenetic clocks showed that epigenetic aging was relatively consistent within individuals. ELA effects were adversity dependent, but each ELA exerted coordinated effects across tissues. Although ELA targeted many of the same loci as age, the directions of effects differed, which indicates that ELA does not uniformly increase epigenetic age. Instead, ELA leaves a coordinated, cross-tissue epigenetic signature that is distinct from-yet intertwined with-age-related differences, which advances our understanding of how early environments sculpt the molecular foundations of aging and disease.
PMID:
42313974
Bibliographic data and abstract were imported from PubMed on 19 Jun 2026.
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