inherently destined to consume low/high amounts of alcohol. Likewise, there are many genes located within these pathways that are differentially expressed between these groups of mice because of variation within and among them. Notably, several of the 3800 unique genes identified in Mulligan’s study (2006) were present in gene loci that had previously been linked to AD in humans. Overall, these approaches point to a physiological domain (linked to metabolism) and a neurological domain (i.e., neuronal profiles susceptibility to alcohol’s effects) that support the pharmacology and neuroscience literature. However, they also indicate complexity in accounting for genetic heterogeneity in association studies as it would require large datasets with extensive phenotyping or alternatively experimental studies that are (1) ethically challenging, (2) experimentally challenging, and (3) fiscally infeasible in humans alone.
