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Author Spotlight: Advancing Alzheimer's Research – Exploring Early Detection and Multi-Omics Approaches
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Decoding nuclear-encoded mitochondrial genes in major depressive disorder: A multi-omics perspective.

Jing Liao1, Xianyan Wang2, Gaokun Dai3

  • 1Department of Child and Adolescent Psychology, Nanchong Psychosomatic Hospital, Nanchong, Sichuan, China.

Psychological Medicine
|November 18, 2025
PubMed
Summary

This study reveals key mitochondrial genes, TDRKH and METAP1D, causally linked to major depressive disorder (MDD) risk through multi-omics analysis. Findings offer new therapeutic targets for MDD.

Keywords:
GWASmajor depressive disordermitochondrial genessummary-based Mendelian randomization

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Area of Science:

  • Genetics
  • Neuroscience
  • Molecular Biology

Background:

  • Mitochondrial dysfunction is linked to major depressive disorder (MDD) pathogenesis.
  • The specific roles of mitochondrial genes in MDD development across regulatory layers are not fully understood.

Purpose of the Study:

  • To investigate the causal involvement of mitochondrial genes in major depressive disorder (MDD) using a multi-omics approach.
  • To identify specific mitochondrial genes and regulatory mechanisms implicated in MDD.

Main Methods:

  • Integrated genome-wide association study (GWAS) data with DNA methylation, gene expression (eQTL), and protein abundance quantitative trait loci (QTL) data.
  • Applied summary-based Mendelian randomization and Bayesian colocalization to assess causal relationships for mitochondrial genes (MitoCarta3.0).
  • Validated findings in brain tissues using Genotype-Tissue Expression (GTEx) eQTL data and prioritized genes based on cross-omics consistency.

Main Results:

  • Five mitochondrial genes were prioritized for their association with MDD.
  • TDRKH showed consistent associations across methylation, transcription, and protein levels, with specific methylation linked to reduced MDD risk.
  • METAP1D demonstrated protective effects at transcript and protein levels, with signals replicated in brain tissues like the cortex.

Conclusions:

  • This study provides multi-omics evidence supporting the causal role of mitochondrial genes in MDD.
  • TDRKH and METAP1D are identified as key candidate genes for MDD.
  • These genes represent promising targets for future mechanistic studies and therapeutic interventions for major depressive disorder.