The Bayesian framework used by ABPA also allows simultaneous estimation of the number of independent SNP loci that contribute to risk for schizophrenia. Here, we assume that the number of genome-wide significant SNP associations and the amount of variance they explain in the Sweden + PGC results reflect only partly the underlying genetic architecture of schizophrenia due to inadequate sample size. Using 1000 Genomes results for Sweden + PGC and assuming population risk of 0.01, we estimated that 8,300 independent SNPs contribute to the genetic basis of schizophrenia and that these SNPs account for 50% of the variance in liability to schizophrenia (95% credible intervals 6,300-10,200 for the number of SNPs and 0.45-0.54 for total variance explained). We stress that these estimates must be interpreted in the context of the assumptions of ABPA and the strengths and weaknesses of the input data. Additional analyses (not shown) indicate that most of the signal was derived from SNPs with allele frequencies > 0.1; low-frequency imputed SNPs were not generally inferred to be associated with schizophrenia. Figure 3 compares ABPA estimates of the
