Our results are consistent with most GWA studies of other quantitative traits in identifying SNPs that explain very small amounts of variance, generally less than 1%, and even these estimates for any particular trait/SNP are likely to be inflated (the “winner's curse”). However, even a SNP that explains a very small amount of variance can guide our understanding of the biological underpinning of complex phenotypes and diseases. Indeed, genetic association tests across the five personality factors point to several SNPs within genes known for their functions in the brain and their effects on behavior and mental disorders (e.g., SNAP-25, CDH13, CDH23, BDNF, CNTNAP2, CLOCK, CTNNA2, IKBKAP, DYRK1A). These findings seem to reflect the phenotypic links between personality and psychiatric disorders. If confirmed in future studies, these findings might also advance our understanding of the continuum between normal and abnormal personality phenotypes. Given the high degree of comorbidity (93, 94) and other limitations of categorical systems (95), a dimensional approach to molecular psychiatry might well provide greater power to detect genetic variants associated with psychiatric disorders, and also provide possible points for eventual pharmaceutical intervention.
