Neuroanatomical dimensions in major depression linked to cognition, adverse life events, self-harm, metabolomics and genetics.
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Xiao Wenyi, Woodham Rachel D, Cui Yuhan, Wen Junhao, Antoniades Mathilde, Srinivasan Dhivya, Fan Yong, Erus Guray, Garcia Jose A, Arnott Stephen R, Chen Taolin, Choi Ki Sueng, Chin Fatt Cherise, Frey Benicio N, Frokjaer Vibe G, Ganz Melanie, Godlewska Beata R, Hassel Stefanie, Ho Keith, McIntosh Andrew M, Qin Kun, Rotzinger Susan, Sacchet Matthew D, Savitz Jonathan, Shou Haochang, Singh Ashish, Stolicyn Aleks, Strigo Irina, Strother Stephen C, Tosun Duygu, Wei Dongtao, Anderson Ian M, Craighead W Edward, Deakin J F William, Dunlop Boadie W, Elliott Rebecca, Gong Qiyong, Gotlib Ian H, Harmer Catherine J, Kennedy Sidney H, Knudsen Gitte M, Mayberg Helen S, Paulus Martin P, Qiu Jiang, Trivedi Madhukar H, Whalley Heather C, Yan Chao-Gan, Young Allan H, Davatzikos Christos, Fu Cynthia H Y
Аннотация
METHODS: Using the semi-supervised machine learning algorithm, Heterogeneity through Discriminative Analysis (HYDRA), we had identified two neuroanatomical dimensions in deeply phenotyped (i.e., comprehensively assessed across neuroimaging, clinical, and behavioural domains), medication-free participants with MDD from the COORDINATE-MDD consortium. In the present study, we apply this pre-trained HYDRA model to the UK Biobank (UKB) to validate these dimensions in a large general population and a subsample with current depressive symptoms.
RESULTS: Dimension 2 (D2), compared to Dimension 1 (D1), is characterized by reduced grey and white matter volumes and limited treatment response to antidepressant and placebo medications. Out-of-sample validation in the UKB general population (n = 37,235) confirms these neuroanatomical features and reveals D2 associations with cognitive impairments, adverse life events, self-harm and suicide attempts, a pro-atherogenic lipid profile, and genetic links to neurodegenerative traits. Similar profiles are observed in the UKB subsample with current depressive symptoms (n = 1455).
CONCLUSIONS: D1 and D2 represent distinct neurobiological mechanisms underlying MDD. The validation in a general population-based cohort and in a cohort sample with depressive symptoms delineates mechanisms underlying heterogeneity in MDD.