RNA sequencing can accurately detect transcription at the gene and isoform level. We sequenced a cohort of SCZ and control subjects that is an order of magnitude larger than prior RNA sequencing studies. By applying state-of-the-art analytic methods and including genome-wide characterization of common variants, we generated a rich resource of the genetics of gene expression in the brain. This resource can serve as a useful catalogue of regulatory variants underlying the molecular basis of SCZ and other brain disorders. We use this resource to identify: (a) specific effects on gene expression of genetic variants previously implicated in risk; (b) genes showing a significant difference in expression between SCZ cases and controls; and (c) coordinated expression of genes implicated in SCZ. Our results shed light on the subtle effects expected from the polygenic nature of SCZ risk and thus substantially refine our understanding of the neurobiology of SCZ.
