Smoking exacerbates amyloid pathology in a mouse model of Alzheimer’s disease

Several epidemiological studies have shown that cigarette smoking might alter the incidence of Alzheimer’s disease. However, inconsistent results have been reported regarding the risk of Alzheimer’s disease among smokers. Previous studies in experimental animal models have reported that administrati...

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Veröffentlicht in:Nature communications 2013-02, Vol.4 (1), p.1495-1495, Article 1495
Hauptverfasser: Moreno-Gonzalez, Ines, Estrada, Lisbell D., Sanchez-Mejias, Elisabeth, Soto, Claudio
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Sprache:eng
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Zusammenfassung:Several epidemiological studies have shown that cigarette smoking might alter the incidence of Alzheimer’s disease. However, inconsistent results have been reported regarding the risk of Alzheimer’s disease among smokers. Previous studies in experimental animal models have reported that administration of some cigarette components (for example, nicotine) alters amyloid-β aggregation, providing a possible link. However, extrapolation of these findings towards the in vivo scenario is not straightforward as smoke inhalation involves a number of other components. Here, we analysed the effect of smoking under more relevant conditions. We exposed transgenic mouse models of Alzheimer’s disease to cigarette smoke and analysed the neuropathological alterations in comparison with animals not subjected to smoke inhalation. Our results showed that smoking increases the severity of some abnormalities typical of Alzheimer’s disease, including amyloidogenesis, neuroinflammation and tau phosphorylation. Our findings suggest that cigarette smoking may increase Alzheimer’s disease onset and exacerbate its features and thus, may constitute an important environmental risk factor for Alzheimer’s disease. A link between smoking and the incidence of Alzheimer’s disease has been implicated in humans. In this study, transgenic mouse models of Alzheimer’s disease exposed to cigarette smoke display increased disease abnormalities in the brain, such as amyloidogenesis, neuroinflammation and tau phosphorylation.
ISSN:2041-1723
2041-1723
DOI:10.1038/ncomms2494