The goal of this paper was to generate hypotheses about potentially causal variants for AD that can be explored further through functional studies. Using an innovative approach, we first deep sequenced entire genes plus flanking regions so that we could explore both common and rare variants and variants located within and outside of exons for association with AD. Next, we formed sets of variants based on biological features that affect protein coding or regulate gene expression, in order to test whether variants with specific features are associated with AD.
