to examine the association between each endophenotype and a) common variants (single nucleotide polymorphisms; SNPs) throughout the genome, b) autosomal genes, c) rare exonic variants, and d) rare and common variants throughout the genome. Our analyses took advantage of improved imputation with a powerful reference panel composed of >1000 moderate-depth whole-genome-sequenced individuals from our own sample. We also targeted specific SNPs, loci, and genes for which there were prior reports indicating they were associated with the endophenotypes, psychopathology related to the endophenotypes, or relevant brain and metabolic systems. Hence, in addition to conducting genome-wide discovery-based analyses, which required correcting for 1 million tests, we followed leads from the literature and tested “hypothesized” subsets of variants within candidate loci and corrected only for those, thus lessening substantially the p-value threshold required for a finding to be considered significant.
