A limitation of this study is that the power to detect significant association signals for small effect sizes is limited by the sample size. This has been clearly demonstrated in many GWAS efforts for other neuropsychiatric conditions (e.g., schizophrenia) in which studies of comparable size have failed to identify significant association signals. Yet, when sample sizes have increased (in some case 10 or more fold), then multiple significant signals were identified. Power was improved in this study by using a hybrid analytic approach that included both family and case-control samples in the analysis. In conclusion, while this OCD GWAS study did not identify a study-wide significant association finding, several of the strongest findings are particularly interesting. There are both plausible biologic hypotheses and prior genetic evidence, for either OCD or related conditions, for the two most significant association findings, PTPRD and CDH9/CDH10. The finding that the signals in this GWAS concur with respect to allele and direction significantly with the top signals in a second reported OCD GWAS, suggests that similar genetic underpinnings of OCD are identified in both studies.
