ArticleBrain, behavior, & immunity - health2025
Adolescent depression, childhood maltreatment, and the immune system; a role for epigenetic aging?
Article in Brain, behavior, & immunity - health, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Transcriptomic characteristics of plasma from Chinese ethnic minority patients with major depressive disorder.Translational psychiatry · 2026Article
- Cross-Platform and cross-species lipidomic profiling identifies promising biomarkers for adolescent major depressive disorder.Molecular psychiatry · 2026Article
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Authors and funding
10 authors.
Funding
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Abstract
Background: Childhood maltreatment is a major risk factor for the development of depression, as well as for imbalances in the immune system, including chronic low-grade inflammation. Less is known about potential immune imbalances in adolescent depression and the role of childhood maltreatment. Furthermore, accelerated epigenetic aging may contribute to the development of inflammation, but has never been examined in the context of adolescent depression. Methods: We investigated childhood maltreatment, inflammation, and epigenetic aging in 78 healthy adolescents and 33 adolescents with a clinically diagnosed depressive disorder. Childhood maltreatment was assessed via self-report, and inflammatory markers (CRP, IL-1β, IL-6, IL-8, sIgA, and TNF-α) were analyzed in saliva. DNA methylation was analyzed in a subsample ( Results: The MANOVA showed that depression was significantly associated with the immune markers, but not with epigenetic aging. Post-hoc tests suggested however that IL-8 levels were reduced, while none of the other markers were affected. Unexpectedly, childhood (emotional) maltreatment was significantly associated with epigenetic age Conclusions: Our results contrast with previous literature in adults, indicating that epigenetic age
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