The propensity to develop AD is strongly influenced by genetics (Rodriguez et al., 1993, Heath et al., 1999, Schuckit and Smith, 1996, Prescott and Kendler, 1999, Schuckit, 2000), and human genetic association studies have identified a variety of candidate loci that are associated with the propensity to develop AD in individual populations (Tawa et al., 2016, Hart and Kranzler, 2015). However, very few of these associations, excepting loci in the ADH and ALDH genes, have been replicated across different studies. One possible reason for the difficulty that has been observed in replicating associations for AD is that traditional replication analysis, in which the same allele or gene is examined in more than one study, presupposes that identical or equivalent mutational events in a given gene must occur across populations to cause the phenotype. This stringent requirement may not appropriately capture the potential role of the gene in AD because it fails to take into account how broader gene networks function. Because genes act together in biological networks to perform a particular function, we reasoned that if a biological process is
