We tested variants in 71 candidate loci plausibly associated with AD. Results showed that no single common variant was associated in any of the loci, which is unsurprising given that we do not have the large sample size needed to detect a small effect of a common variant ( N > 10,000). This is also consistent with other GWASs of AD where either no variants were found to be significantly associated or the associated variants only explained a small portion of AD risk(Hart and Kranzler, 2015). We then tested if sets of variants formed on the basis of overlap with biologically meaningful annotations within a given locus were associated with AD. These analyses identified sets overlapping with potentially functional (affecting protein coding or regulatory processes) annotations that were significantly associated with AD.
