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Cortical patterning of abnormal morphometric similarity in psychosis is associated with brain expression of schizophrenia-related genes
Author(s) -
Sarah E. Morgan,
Jakob Seidlitz,
Kirstie Whitaker,
Rafael Romero-García,
Nicholas E. Clifton,
Cristina Scarpazza,
Thérèse van Amelsvoort,
Machteld Marcelis,
Jim van Os,
Gary Donohoe,
David Mothersill,
Aiden Corvin,
Andrew Pocklington,
Armin Raznahan,
Philip McGuire,
Petra E. Vértes,
Edward T. Bullmore
Publication year - 2019
Publication title -
proceedings of the national academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.1820754116
Subject(s) - schizophrenia (object oriented programming) , psychosis , neuroimaging , similarity (geometry) , neuroscience , gene , phenotype , biology , genetic similarity , gene regulatory network , gene expression , psychology , genetics , medicine , psychiatry , population , artificial intelligence , computer science , environmental health , genetic diversity , image (mathematics)
Schizophrenia has been conceived as a disorder of brain connectivity, but it is unclear how this network phenotype is related to the underlying genetics. We used morphometric similarity analysis of MRI data as a marker of interareal cortical connectivity in three prior case-control studies of psychosis: in total, n = 185 cases and n = 227 controls. Psychosis was associated with globally reduced morphometric similarity in all three studies. There was also a replicable pattern of case-control differences in regional morphometric similarity, which was significantly reduced in patients in frontal and temporal cortical areas but increased in parietal cortex. Using prior brain-wide gene expression data, we found that the cortical map of case-control differences in morphometric similarity was spatially correlated with cortical expression of a weighted combination of genes enriched for neurobiologically relevant ontology terms and pathways. In addition, genes that were normally overexpressed in cortical areas with reduced morphometric similarity were significantly up-regulated in three prior post mortem studies of schizophrenia. We propose that this combined analysis of neuroimaging and transcriptional data provides insight into how previously implicated genes and proteins as well as a number of unreported genes in their topological vicinity on the protein interaction network may drive structural brain network changes mediating the genetic risk of schizophrenia.

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