Presumably, complex biological mechanisms are responsible for SD, and the heterogeneity of SD phenotypes reflects the existence of a spectrum of diseases with different mechanisms. The co-existence of many different SD disorders in an individual is common clinically; in the United States, the odds ratio of comorbid DD with AD, adjusted for demographic characteristics, is as high as 18.7 (Compton et al., 2007). Narrowing down the shared and specific genetic risk factors for different SD disorders would help to understand the biology of this multifaceted set of disorders. To advance such an understanding, in this study, we investigated the association of the NTAD gene cluster with comorbid of AD+DD, or AD alone.
