disorder (0.32; P = 5.4 × 10−6) and for schizophrenia and bipolar disorder coheritability (0.37; P = 8.5 × 10−8) (Fig. 2 and Supplementary Table 3). For other disorders or pairs of disorders, the estimates explained by CNS+ SNPs did not differ from the values expected by chance (Supplementary Table 3), although their large standard errors suggest that we cannot address this question with precision. For data from the schizophrenia and bipolar disorder pair, we also partitioned the heritabilities explained by SNPs by minor allele frequency (MAF) (Supplementary Table 4) and by chromosome (Supplementary Fig. 1). The high standard errors on estimates limited interpretation, but the results are consistent with a polygenic architecture comprising many common variants of small effect dispersed throughout the genome. The MAF partitioning suggests that a key part of the variance explained by SNPs is attributable to common causal variants (this was investigated in detail for schizophrenia35), but the low contribution to the total variance explained by SNPs with MAF of <0.1 reflects, at least in part, under-representation of SNPs with low MAFs in the analysis (minimum MAF = 0.01) relative to those present in the genome.
