Evidence mapPaperPMID 42387104Full record

ArticleMolecular psychiatry2026

Cross-ancestry pleiotropic analysis of imaging-derived phenotypes enhances risk stratification of depression.

Yu Feng, Xiaonan Guo, Peng Huang, Ningning Jia, Shaohua Hu, Sheng Yang

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Article in Molecular psychiatry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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6 authors.

Yu Feng *Department of Psychiatry, the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Xiaonan Guo *Department of Psychiatry, the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.ORCID http://orcid.org/0000-0002-0801-6133
Peng Huang *Department of Epidemiology, Centre for Global Health, School of Public Health, National Vaccine Innovation Platform, Key Laboratory of Public Health Safety and Emergency Prevention and Control Technology of Higher Education Institutions in Jiangsu Province, Nanjing Medical University, Nanjing, Jiangsu, 211166, China.
Ningning JiaLiangzhu Laboratory, Zhejiang University Medical Center, Hangzhou, China.
Shaohua HuDepartment of Psychiatry, the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China. dorhushaohua@zju.edu.cn.ORCID http://orcid.org/0000-0003-0570-670X
Sheng YangDivision of Pediatric Pulmonary Medicine, UPMC Children's Hospital of Pittsburgh, University of Pittsburgh, Pittsburgh, PA, 15224, USA. shy229@pitt.edu.ORCID http://orcid.org/0000-0003-3657-8771

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Depression arises from dynamic interactions among genetic predisposition, brain alterations, and environmental stressors. Despite genome-wide association studies (GWAS) identifying risk loci, the mechanisms translating genetic variation into brain changes remain elusive. Imaging-derived phenotypes (IDPs) were the intermediate traits linking genetic architecture to neural circuit dysfunction. Here, we collected large-scale GWAS summary statistics of depression and IDPs across European (EUR; N = 1,293,933 and 33,224, respectively) and East Asian (EAS; N = 82,874 and 7058, respectively). In the multiple-trait analysis between depression and IDPs, we clarified their genetic correlation through MTAG, identified the pleiotropic single nucleotide variants (SNVs) and genes with functional insight, and established the causal relationship through Mendelian randomization via TwoSampleMR in EUR and EAS ancestry, respectively. To discern the heterogeneous genetic drivers, we selected independent SNVs from the multiple-trait analyses to perform unsupervised clustering. Six clusters delineated distinct biological pathways for metabolic regulation, neurotransmitter dynamics, and neuroimmune interactions, with tissue/cell type specificity through MAGMA. Finally, we dissected relationships between depression and polygenic risk score, IDPs, and modifiable lifestyle factors, and introduced a machine learning framework to refine risk stratification (N = 16,166). Our study advanced the understanding of the multiscale etiology of depression while providing dynamic depression risk stratification for precision prevention.

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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 Socratic graph.