In conclusion, we report that a significant proportion of variance in AD risk can be explained by common SNPs of small effect in an aggregate manner, with allelic architectures that are specific to EA and AA populations. Although these findings would appear to support the widely held common disease-common variant hypothesis, our simulation models show that the modest effects of rare and uncommon susceptibility loci can be captured in genome-wide association signals for complex disease phenotypes, at least in aggregate. How big of a role rare variation actually has, if any, in the genetic liability of alcoholism is unknown, however there is growing evidence that it can have important effects on psychiatric disorders, including results from studies of copy number variants (CNVs) (Stone et al. 2008; Sanders et al. 2011), as well as early findings from exome sequencing efforts that reveal an abundance of rare genetic variation, much of which is functional (Keinan & Clark 2012; Kiezun et al. 2012; Tennessen et al. 2012). In addition, our GWAS data sets have implicated a number of biologically relevant pathways and mechanisms
