Our findings should be considered within the context of a few key limitations. First, despite being large, it is evident that our sample is underpowered to detect loci of modest effect. However, our sample was considerably larger than in our prior efforts in a subset of these data (e.g., 7-9) and one GWS SNP from those prior studies, previously linked to a latent class representing high-risk for AD9, continued to be nominally associated with DSM-IV AD in the current analysis (rs17484734, prior p =4.1E-8, current p=8.77E-5) but two other borderline significant variants were not as strongly associated in the current larger sample (rs11035102, for Desire to cut back9: prior p = 7.3E-8, current p=0.002; rs12903120, for AD criterion count8: prior p=5.45E-8, current p=0.03). Second, some of our GWS loci had low minor allele frequencies which may also have limited replication efforts. Third, our AA subsample, while utilized in the EA+AA analysis, was too small to report on individually, due to the strict definition of AD affecteds. Larger discovery GWAS of non-EA samples is much needed.
