Objectives: Schizophrenia genetics is complex, and the contribution of common and rare variants are not fully understood. Several specific copy number variations (CNVs) confer increased risk, and the study of their effects is central to molecular models of mental disorders. However, these CNVs are spread across the genome and differ in the number of genes affected and classes of coded proteins. This diversity suggests that we need to look beyond the deleted or duplicated genes, to their interaction partners and involved molecular pathways.
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Ehrhart et al. (2024) studied this question.
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