INTRODUCTIONGenome‐wide association studies (GWAS) of schizophrenia (SZ) have so far identified 108 regions of DNA encompassing ∼350 genes. A strongly polygenic model of SZ, where the overall influence of many genes of small effect combine to increase an individual's predisposition to SZ has been robustly supported (Purcell et al., ). No one “schizophrenia gene” of large effect has been identified, with the number of genes associated with the disorder increasing as GWAS sample size increases. This interplay of SZ risk genes is important to study, given the polygenic nature of the disorder. To characterize the phenotypic effects of multiple risk variants we and others have used polygenic risk scores calculated for gene sets based on either their involvement in a known biological pathway (Hargreaves et al., ), or based on evidence of their being regulated by target risk genes, for example, ZNF804A (Nicodemus et al., ); MIR137 (Cosgrove et al., ). In these studies, similar effects on cognitive function have been observed by studying either the risk variant individually or the gene network with which it interacts, although the network based analysis can sometimes explain a slightly higher percentage of variation (Cosgrove et al., ).Genetic variants within the gene
American Journal of Medical Genetics – Wiley
Published: Jan 1, 2018
Keywords: ; ; ;
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