In conclusion, this study provides substantial evidence that both TS and OCD are highly heritable, polygenic, and that a significant majority of the heritability of both disorders is captured by GWAS SNP variants. Using both directly genotyped and imputed data, we also provide evidence of allelic architecture differences between TS and OCD. Specifically, we identified a significant contribution from rare variants in the genomic architecture of TS that appears to be absent from the architecture of OCD. Our results also provide additional evidence of a prominent role for chromosome 15 in OCD liability and possible concentration of TS liability on chromosomes 2, 5, 11, 12, 16 and 20. We also find that brain eQTLs concentrate a significant proportion of the heritability present in TS and OCD. It is unlikely that the differences in genetic architecture between TS and OCD are due to incomplete matching during QC or other, unknown, technical biases, as all cases were genotyped with identical technology, shared the same control set, and were imputed together. Taken together, these results advance our understanding of the overlapping and non-overlapping
