Early exposure to stress is associated with biological processes that precede cellular senescence and an increased risk of age-related diseases. Adolescence is a period of heightened susceptibility to social environment-related stressors. This developmental stage is also associated with the onset of psychiatric disorders and the adoption of behaviors that can affect long-term health trajectories. In this review, we aimed to assess the progress of rodent research on the relationship between adolescent social stress and later disease-related sequels and cellular senescence. We present a synthesis of 35 peer-reviewed articles indexed in PubMed before July 2025, selected from a web search based on the terms (social stress) AND (senescence OR DNA damage OR telomere OR inflammation) AND (adolescence OR juvenile OR youth OR early life) AND (mice OR mouse OR murine OR rat OR rodent). Adolescent social stress results in decreased social behaviors and increased anxietylike and depressionlike responses. In addition, enduring alterations in physiological responses to acute stress challenges and broad sequelae on neural, cardiovascular, endocrine, and gastrointestinal systems associated with inflammation were found. Sex differences in stress susceptibility were observed across all domains. However, despite the theoretical framework linking stress to aging, our synthesis reveals that direct evidence regarding telomere dynamics and DNA damage in this specific developmental window remains limited in rodent research. Consequently, this review provides an overview of biological mechanisms linking psychosocial stress during adolescence to chronic disease states while identifying the scarcity of direct senescence data as an important gap for future investigation. (PsycInfo Database Record (c) 2026 APA, all rights reserved).
Novoa et al. (Thu,) studied this question.