We obtained genome-wide genotype data from which we constructed 49 ancestry matched, non-overlapping case-control samples (46 of European and three of East Asian ancestry, 34,241 cases and 45,604 controls) and 3 family-based samples of European ancestry (1,235 parent affected-offspring trios) (Supplementary Table 1 and Supplementary text). These comprise the primary PGC GWAS dataset. Genotypes from all studies were processed by the PGC using unified quality control procedures followed by imputation of SNPs and insertion-deletions using the 1000 Genomes Project reference panel.25 In each sample, association testing was conducted using imputed marker dosages and principal components (PCs) to control for population stratification. The results were combined using an inverse-weighted fixed effects model.26 After quality control (imputation INFO score ≥ 0.6, MAF ≥ 0.01, and successfully imputed in ≥ 20 samples), we considered around 9.5 million variants. The results are summarized in Figure 1. To enable acquisition of large samples, some groups ascertained cases via clinician diagnosis rather than a research-based assessment and provided evidence of the validity of this approach (Supplementary text).11,13 Post-hoc analyses revealed the pattern of effect sizes for
