ArticleNeuroscience applied2025
Telomere length and mitochondrial DNA copy number in association with trauma-focused psychotherapy efficacy.
Article in Neuroscience applied, 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.
- Study on the cognitive effects of eye movement desensitization and reprocessing: proposed active mechanisms.Frontiers in computational neuroscience · 2026Article
- Progress and developments in pharmacogenomics and pharmacoepigenomics discovery and translation for the personalization of pharmacological treatments in psychiatric disorders.Neuroscience applied · 2024Article
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Authors and funding
14 authors.
Funding
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Abstract
Early life adversities (ELA) have been linked to a greater risk for major depressive disorder (MDD) and treatment-resistant depression (TRD). The molecular mechanisms underlying the link between ELA and MDD and/or TRD are yet unknown. It has been suggested that ELA induces an allostatic burden, which in turn promotes oxidative stress and an inflammatory response that are further intensified by the influence of maladaptive coping behaviour. In this study we explored the role of two markers of cellular aging and oxidative stress (leukocyte telomere length (LTL) and mitochondrial DNA copy number (mtDNAcn)) in TRD and in response to trauma-focused psychotherapies. The study comprised 30 TRD patients receiving trauma-focused psychotherapies and 65 healthy controls. LTL and mtDNAcn were measured at baseline and four weeks after the end of the psychotherapy sessions. Response was defined based on reduction in the Montgomery-Åsberg Depression Rating Scale (MADRS). In the case control analysis, the logistic regression model showed that mtDNAcn but not LTL was a significant predictor of diagnosis (chi-square 92.108, p = 7.72e-20; contribution of mtDNAcn, B = -9-297, p = 0.00009). In the TRD sample, LTL and mtDNAcn were inversely correlated with MADRS score at baseline (LTL, Pearson's r = -0.478, p = 0.008; mtDNAcn, Pearson's r = -0.656, p = 0.00008), but there was no difference in either LTL or mtDNAcn between responders and non-responders. In conclusion, our findings support an involvement of cellular aging in TRD, and suggest that LTL and mtDNAcn are not predictors or mediators of response to trauma-focused psychotherapies.
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