The negative impact of alcohol intake on mitochondrial function has been well documented in several animal models, and excessive alcohol consumption in mice has been linked to degradation of mitochondrial DNA [66–69]. As AD is a risk factor for dementia, prolonged alcohol consumption has been shown to have a toxic effect on amyloid precursor protein. This leads to an accumulation of beta-amyloid in neurons from alcohol dependent rats, perhaps mediated through increased production of reactive oxygen species and mitochondrial dysfunction [70]. Results from human studies, however, have been more equivocal. While a postmortem brain analysis of chronic alcoholics did not detect greater incidence of neuropathological lesions compared to control subjects, a Swedish national cohort study concluded that history of alcohol dependence conferred a greater risk for Parkinson’s disease diagnosis [71, 72].
