Despite the advances, there is a long way to go to fully characterize the genetic basis for AD, and while it is likely that linkage and candidate gene or targeted association analysis will not take us the rest of the way, it is also now the case that these methods are rapidly being augmented by newer methodologies. These include, but are not limited to, GWAS, study of copy number variation (CNV) (where CNV of the alcohol-metabolizing enzymes would be an obvious possible source of risk variance), and deep sequencing of candidate loci with the goal of identifying rare risk-influencing variants. We can reasonably hope that as this technology is applied to AD, more small-to-medium-effect risk loci will be identified.
