Virtual Ontogeny of Cortical Growth Preceding Mental Illness

Yash Patel, Jean Shin, Christoph Abé, Ingrid Agartz, Clara Alloza, Dag Alnæs, Sonia Ambrogi, Linda A Antonucci, Celso Arango, Volker Arolt, Guillaume Auzias, Rosa Ayesa-Arriola, Nerisa Banaj, Tobias Banaschewski, Cibele Bandeira, Zeynep Başgöze, Renata Basso Cupertino, Claiton H D Bau, Jochen Bauer, Sarah BaumeisterFabio Bernardoni, Alessandro Bertolino, Caterina Del Mar Bonnin, Daniel Brandeis, Silvia Brem, Jason Bruggemann, Robin Bülow, Juan R Bustillo, Sara Calderoni, Rosa Calvo, Erick J Canales-Rodríguez, Dara M Cannon, Susanna Carmona, Vaughan J Carr, Stanley V Catts, Sneha Chenji, Qian Hui Chew, David Coghill, Colm G Connolly, Annette Conzelmann, Alexander R Craven, Benedicto Crespo-Facorro, Kathryn Cullen, Andreas Dahl, Udo Dannlowski, Christopher G Davey, Christine Deruelle, Covadonga M Díaz-Caneja, Katharina Dohm, David Willinger

Research output: Journal article (peer-reviewed)Journal article

4 Citations (Scopus)

Abstract

BACKGROUND: Morphology of the human cerebral cortex differs across psychiatric disorders, with neurobiology and developmental origins mostly undetermined. Deviations in the tangential growth of the cerebral cortex during pre/perinatal periods may be reflected in individual variations in cortical surface area later in life.

METHODS: Interregional profiles of group differences in surface area between cases and controls were generated using T1-weighted magnetic resonance imaging from 27,359 individuals including those with attention-deficit/hyperactivity disorder, autism spectrum disorder, bipolar disorder, major depressive disorder, schizophrenia, and high general psychopathology (through the Child Behavior Checklist). Similarity of interregional profiles of group differences in surface area and prenatal cell-specific gene expression was assessed.

RESULTS: Across the 11 cortical regions, group differences in cortical area for attention-deficit/hyperactivity disorder, schizophrenia, and Child Behavior Checklist were dominant in multimodal association cortices. The same interregional profiles were also associated with interregional profiles of (prenatal) gene expression specific to proliferative cells, namely radial glia and intermediate progenitor cells (greater expression, larger difference), as well as differentiated cells, namely excitatory neurons and endothelial and mural cells (greater expression, smaller difference). Finally, these cell types were implicated in known pre/perinatal risk factors for psychosis. Genes coexpressed with radial glia were enriched with genes implicated in congenital abnormalities, birth weight, hypoxia, and starvation. Genes coexpressed with endothelial and mural genes were enriched with genes associated with maternal hypertension and preterm birth.

CONCLUSIONS: Our findings support a neurodevelopmental model of vulnerability to mental illness whereby prenatal risk factors acting through cell-specific processes lead to deviations from typical brain development during pregnancy.

Original languageEnglish
Pages (from-to)299-313
Number of pages15
JournalBiological Psychiatry
Volume92
Issue number4
DOIs
Publication statusPublished - 15 Aug 2022
Externally publishedYes

Keywords

  • Attention Deficit Disorder with Hyperactivity
  • Autism Spectrum Disorder/genetics
  • Bipolar Disorder
  • Cerebral Cortex
  • Child
  • Depressive Disorder, Major/pathology
  • Female
  • Humans
  • Infant, Newborn
  • Magnetic Resonance Imaging/methods
  • Pregnancy
  • Premature Birth/pathology

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