ArticlePsychological medicine2026
Controllability of morphometric network colocalize with underlying neurobiology in major depression.
Article in Psychological medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Transcriptional signatures of cortical morphometric variability in temporal lobe epilepsy.Epilepsia open · 2026Article
- Bridging molecules and connectome: network biomarkers guided by neurotransmitter architecture in major depressive disorder.Translational psychiatry · 2026Article
- Cortical morphometric inverse divergence in attention-deficit/hyperactivity disorder correlates with cell-type-specific, laminar-specific and developmental transcriptomic signatures.Psychological medicine · 2026Article
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11 authors.
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Abstract
backgroundCognitive and behavioral symptoms of major depressive disorder (MDD) are linked to aberrant changes in the controllability of brain networks. However, previous studies examined network controllability using white matter tractography, neglecting the contributions of gray matter. We aimed to examine differences in the controllability of morphometric networks between patients with MDD and demographic-matched healthy controls and identify the associated neurobiological signatures.
methodsBased on the structural and diffusion MRI data from two independent cohorts, we calculated the controllability of morphometric similarity networks for each participant. A generalized additive model was used to investigate the case-control differences in regional controllability and their cognitive and behavioral associations. We investigated the associations between imaging-derived controllability and neurotransmitters, brain metabolism, and gene transcription profiles using multivariate linear regression and partial least squares regression analyses.
resultsIn both cohorts, depression-related abnormalities of morphometric network controllability were primarily located in the prefrontal, cingulate, and visual cortices, contributing to memory, sensation, and perception processes. These abnormalities in network controllability were spatially aligned with the distributions of serotonergic transmission pathways as well as with altered oxygen and glucose metabolism. In addition, these abnormalities spatially overlapped with differentially expressed genes enriched in annotations related to protein catabolism and mitochondria in neuronal cells and were disproportionately located on chromosome 22.
conclusionsCollectively, neuroimaging evidence revealed aberrant morphometric network controllability underlying MDD-related cognitive and behavioral deficits, and the associated genetic and molecular signatures may help identify the neurobiological mechanisms underlying MDD and provide feasible therapeutic targets.
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