Despite evidence from biometric analyses and GCTA that additive genetic influences on P3 amplitude and the P3 genetic factor score are substantial and due in large part to common variants, we failed to obtain genome-wide significant associations with any individual SNPs for either endophenotype, including those in our sets of candidate SNPs selected for having been reported to be associated with P3 amplitude or P3-related activity in previous genome-wide studies or because they are hypothesized to be relevant to disorders associated with our endophenotypes.
