Absence of effect of chronic nicotine administration on amyloid beta peptide levels in transgenic mice overexpressing mutated human APP (Sw, Ind)

Document Type

Article

Abstract

Studies have indicated that nicotine has disease-modifying and cognitive-enhancing properties in Alzheimer's disease (AD). Nicotine has been proposed to be neuroprotective through anti-amyloid beta (Aβ) effects, anti-excitotoxic effects, and anti-free radical effects. Previously, conflicting data from Aβ plaque developing transgenic mice have shown significant Aβ-lowering effects, or alternatively no effects, of nicotine administration. In this study, dosing of transgenic mice (J20 strain) with mutated human APP (Swedish mutations: K670N and M671L and Indiana mutation: V717F) transgene, with nicotine in drinking water for 20 weeks did not have a significant effect on total levels of Aβ 40 or 42 in hippocampus or cortex. This treatment strategy resulted in increased levels of nicotinic acetylcholine receptor activity, and reduced levels of cortical glial fibrillary acidic protein, but had no effect on cortical synaptophysin protein levels. The J20 mouse strain produces higher levels of Aβ 42, the more pathogenic form of Aβ, than Aβ 40 compared to other Aβ plaque developing mouse strains; this could account for differences in effectiveness of nicotine in transgenic mice models of AD. © 2008 Elsevier Ireland Ltd. All rights reserved.

Publication Date

12-26-2008

Publication Title

Neuroscience Letters

ISSN

03043940

Volume

448

Issue

2

First Page

217

Last Page

220

PubMed ID

18926877

Digital Object Identifier (DOI)

10.1016/j.neulet.2008.10.004

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