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Lookup NU author(s): Roslyn Hall, Emeritus Professor Elaine Perry, Dr Jennifer Court
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Alzheimer's disease neuropathology is characterised by beta-amyloid plaques and neurofibrillary tangles. Inhibition of beta-amyloid accumulation may be essential for effective therapy in Alzheimer's disease. In this study we have treated transgenic mice carrying the Swedish mutation of human amyloid precursor protein [Tg(Hu.APP696X670N-M671L)25761, which develop brain beta-amyloid deposits, with nicotine in drinking fluid (200 mug/mL) from 9-14.5 months of age (5.5 months). A significant reduction in amyloid beta peptide 1-42 positive plaques by more than 80% (p < 0.03) was observed in the brains of nicotine treated compared to sucrose treated transgenic mice. In addition, there was a selective reduction in extractable amyloid β peptides in nicotine treated mice; cortical insoluble 1-40 and 1-42 peptide levels were lower by 48 and 60%, respectively (p < 0.005), whilst there was no significant change in soluble 1-40 or 1-42 levels. The expression of glial fibrillary acidic protein was not affected by nicotine treatment. These results indicate that nicotine may effectively reduce amyloid beta peptide aggregation in brain and that nicotinic drug treatment may be a novel protective therapy in Alzheimer's disease.
Author(s): Hall R; Perry E; Court J; Nordberg A; Hellstrom-Lindahl E; Lee M; Johnson M; Mousavi M; Bednar I
Publication type: Article
Publication status: Published
Journal: Journal of Neurochemistry
Year: 2002
Volume: 81
Issue: 3
Pages: 655-658
ISSN (print): 0022-3042
ISSN (electronic): 1471-4159
Publisher: Wiley-Blackwell Publishing Ltd.
URL: http://dx.doi.org/10.1046/j.1471-4159.2002.00874.x
DOI: 10.1046/j.1471-4159.2002.00874.x
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