cortex and amygdala of mice, which suggests that alcohol use may promote vulnerability to AD-like pathology. Second, we present results from original preclinical studies designed to evaluate the impact of nondependent alcohol drinking on AD-like neural and behavioral pathology using the triple-transgenic mouse model of AD (3xTg-AD), which expresses human Tau, APP, and PSEN-1 transgenes. This novel work suggests that alcohol use may exacerbate the onset and magnitude of AD-like pathology in vulnerable individuals. Research that focuses on the impact of alcohol use and abuse on specific molecular mechanisms of AD will move the field forward in understanding potentially unique age-dependent vulnerability in older individuals.
