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Smoking exacerbates amyloid pathology in a mouse model of Alzheimer's disease
- Source :
- NATURE COMMUNICATIONS, Artículos CONICYT, CONICYT Chile, instacron:CONICYT
- Publication Year :
- 2012
-
Abstract
- 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-b 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.
- Subjects :
- Genetically modified mouse
Amyloid pathology
medicine.medical_specialty
Amyloid
Smoke inhalation
General Physics and Astronomy
Mice, Transgenic
tau Proteins
Disease
General Biochemistry, Genetics and Molecular Biology
Nicotine
Mice
Alzheimer Disease
Epidemiology
Glial Fibrillary Acidic Protein
Presenilin-1
Medicine
Animals
Humans
Gliosis
Phosphorylation
Cotinine
Neuroinflammation
Multidisciplinary
Amyloid beta-Peptides
business.industry
Smoking
General Chemistry
medicine.disease
Disease Models, Animal
Immunology
Nerve Degeneration
Environmental Risk Factor
Microglia
business
medicine.drug
Subjects
Details
- ISSN :
- 20411723
- Volume :
- 4
- Database :
- OpenAIRE
- Journal :
- Nature communications
- Accession number :
- edsair.doi.dedup.....ed90267ed7fdae3e9cb50bac636fe847