In an effort to further understand the genomic architecture of OCD and TS, we performed exploratory analyses of heritability across the MAF spectrum. By running all MAF bins together in a single REML analysis, we partitioned the effects of LD across each bin, as Lee et al (2012) previously demonstrated through simulation that this approach restricts the effects of LD between bins and reflects expected heritability per bin based on simulated risk allele distributions. For OCD, no heritability was captured by SNPs with MAF<5%, while the majority of the heritability detected was due to those SNPs with MAF>30%. In contrast, for TS, 21% of the total heritability was captured by SNPs with MAF less than 5% with the remaining bulk of the heritability shared approximately equally among alleles with MAF between 0.10–0.50. Analysis of imputed data confirmed these findings and showed that SNPs with MAF<0.05 accounted for 30% of the total TS heritability and 0% of the total OCD heritability. To ensure that the difference between TS and OCD rare SNP heritability estimates were not due to subtle population substructure
