To identify SNPs and genes that might be causally linked to the genome-wide significant associations, we used FINEMAP39 to identify credibly causal alleles (those with a cumulative posterior probability for a locus of at least 95%) and functionally annotated these alleles using ANNOVAR40. This identified 6,105 credible SNPs across 144 genome-wide significant loci, excluding the major histocompatibility complex (MHC) region (Methods and Supplementary Table 11). From these, we defined a highly credible set of SNPs (n = 25) as those that were more likely to explain the associations than all other SNPs combined (i.e., with a FINEMAP posterior probability greater than 0.5). Of these, 14 mapped to genes on the basis of putative functionality (exonic SNPs that cause nonsynonymous or splice variations or promoter SNPs; n = 6) or mapped to regions identified as likely regulatory elements (n = 8) through chromosome conformation analysis performed in tissue from the developing brain using Hi-C41 physical interactions (Methods and Supplementary Table 12). One of the implicated alleles was a nonsynonymous variant in the manganese and zinc transporter gene SLC39A8. Nonsynonymous variants in
