Molecular genetic studies have the potential to more clearly and more powerfully distinguish genetic from environmental factors. Recent molecular genetic studies have identified a substantial polygenic component to SCZ risk involving hundreds to thousands of common alleles of small effect, and this component was shown to also contribute to risk of BP (12). This analysis pointed to risk shared across many genetic markers, but results from individual genome-wide association studies (GWAS) have also implicated specific common shared loci (13). Taking this further, in a meta-analysis of most of the world’s available GWAS data, the Psychiatric Genomic Consortium Bipolar and Schizophrenia Working Groups identified SNPs for both BP and SCZ in CACNA1C, ANK3 and ITIH3-ITIH4 as genome wide significant but not in MHC, ODZ4, TCF4 and other loci that were genome-wide significant for either disorder separately. Additionally, the Cross-Disorder Group of the Psychiatric Genomics Consortium explicitly tested SNPs across five disorders for the best fitting disease model and identified CACNA1C as more significantly associated to a model combining only BP and SCZ than one including other disorders (14).
