Alzheimer-like pathology in rat receiving passive smoking

Abstract

Although epidemiological studies shows that smoking could increase the risk of Alzheimer’s disease (AD), the molecular basis linking smoking with increased incidence of AD is still unclear. We have established a model of passive smoking (1 hour per day exposure to either sham air or 4% cigarette smoke) for 8 weeks in the ventilated smoking chamber on Sprague-Dawley rats and investigated the changes of β-amyloid (Aβ) in the model. It was found that smoke exposure resulted in increased accumulation of Aβ, up-regulation of β amyloid precursor protein (APP), its proteolytic product sAPPβ fragment as well as β-site APP-cleaving enzyme 1 (BACE1). In addition, the level of nitrotyrosine, a marker of oxidative stress, and 8-hydroxyguanosine, a marker of oxidative damage, was found to be significantly increased in the hippocampus of passive smoking rats. Taken together, our data suggest that passive smoking can induce Alzheimer-like Aβ pathology, and this pathological event may be associated with increased oxidative stress. Our study provides compelling evidence to support the findings from epidemiological studies.