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

被引:91
|
作者
Moreno-Gonzalez, Ines [1 ]
Estrada, Lisbell D. [2 ,3 ]
Sanchez-Mejias, Elisabeth [4 ]
Soto, Claudio [1 ]
机构
[1] Univ Texas Med Sch Houston, Dept Neurol, Mitchell Ctr Alzheimers Dis & Related Brain Disor, Houston, TX USA
[2] Pontificia Univ Catolica Chile, Lab Senalizac Celular, Santiago, Chile
[3] Univ Bernando OHiggins, Santiago, Chile
[4] Univ Malaga, CIBERNED, Dept Cell Biol, E-29071 Malaga, Spain
来源
NATURE COMMUNICATIONS | 2013年 / 4卷
关键词
CIGARETTE-SMOKING; RISK-FACTOR; COGNITIVE DECLINE; NICOTINE; DEMENTIA; COTININE; PROTEIN; MIDLIFE; BRAINS; MEMORY;
D O I
10.1038/ncomms2494
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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-beta 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.
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页数:10
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