Imaging investigations of alcohol-related brain disorders show unique neuropathology (as outlined in table 1), offering a framework for examining pathology in uncomplicated alcoholism. Because brains affected by AUD can show mild effects in the regions aggressively targeted by overt disease, animal models have been useful in distinguishing the etiology of pathology and differentiating brain regions specifically targeted by thiamine deficiency versus hyperammonemia, for example. Individuals with AUD may show more prominent effects in some regions compared with others, suggesting a propensity for one diagnosis over another (e.g., an alcoholic may be more vulnerable to thiamine deficiency than to liver damage). What remains unresolved, and what animal models can help determine, is why certain brain regions are differentially vulnerable to certain pathologies. For example, are the colliculi sensitive to thiamine deficiency because of their relatively high metabolic rate (Landau et al. 1955; Sokoloff et al. 1977)? Is the pons susceptible to CPM because of its proximity to the basilar artery? Does dopamine explain why basal ganglia are targets of liver disease (Mousseau et al. 1993)?
