ArticleBiological psychiatry global open science2025
Decreased Mitochondrial DNA Integrity and Elevated Inflammatory Markers in Late-Life Depression: A Longitudinal Study.
Article in Biological psychiatry global open science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- From inflammaging to precision psychiatry: metabolic-immune crosstalk as a driver of late-life depression trajectories.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Identification of an immune-metabolic biosignature linking depressive symptoms and breast cancer in a clinical population.Translational psychiatry · 2026Article
- Integrative In Silico Analysis of miRNA-mRNA Regulatory Networks in the Prefrontal Cortex of Individuals with Psychiatric Disorders Who Died by Suicide.International journal of molecular sciences · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Background: Late-life depression (LLD) is a prevalent and severe mental disorder. The biological mechanisms underlying LLD are not fully understood, but increasing evidence suggests that mitochondria play a significant role. Impaired mitochondrial function leads to excessive production of reactive oxygen species and the release of circulating cell-free mitochondrial DNA (ccf-mtDNA). The ccf-mtDNA activates the toll-like receptor system, which triggers a systemic proinflammatory response. However, there is limited understanding of the impact of ccf-mtDNA integrity, such as deletions, on LLD pathological conditions. Methods: We included 90 older individuals (50 LLDs, 40 nondepressed healthy control participants [HCs]), with a subset of individuals followed up at 30 months (13 LLDs, 13 HCs). Plasma was separated from blood, and DNA was extracted. Mitochondrial genes MT-ND2 and MT-ND4 were targeted to evaluate ccf-mtDNA levels and deletion using real-time quantitative polymerase chain reaction. Plasma interleukins (ILs) 1β, 5, and 6 were quantified via multiplex immunoassay. Results: LLD was linked to increased ccf-mtDNA instability at baseline (deletion: Conclusions: Increased ccf-mtDNA instability may heighten vulnerability to emotional dysregulation and medical burden in individuals with LLD. Further research is needed to validate our findings and elucidate the mechanisms that connect mitochondrial instability and inflammation in LLD.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.