of this structure in AD-associated behavioral pathologies (Masurkar, 2018); thus, subregional and circuit analyses have potential to identify specific anatomical substrates of alcohol’s impact on AD. Given the involvement of these brain regions in the onset of AD-like pathology, attenuating activity of this pathway may block or enhance disease state. Future studies might also pursue alcohol-induced instability of the Alzheimer’s-linked neural proteome or assess other mouse models of the disease. Additional approaches such as rodent fMRI to assess functional connectivity among AD target brain regions may also reveal novel neural pathways and mechanisms that are targeted by alcohol in AD-vulnerable or AD-expressing populations. Mechanistic studies are highly difficult, or even improbable, to conduct in human subjects; thus, further underscoring the value of having a well-characterized mouse model of AD to evaluate the impact of alcohol use on disease progression. Overall, mouse models of AD offer a novel and an exciting approach to assess the impact of alcohol use on neurodegeneration and represent an opportunity to identify novel therapeutic targets that could have long-lasting beneficial health consequences for the elderly population.
