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Neurosci Lett. 2011 Feb 18;490(1):16-20. doi: 10.1016/j.neulet.2010.12.017. Epub 2010 Dec 16.

Lead exposure increases levels of β-amyloid in the brain and CSF and inhibits LRP1 expression in APP transgenic mice.

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  • 1Department of Neurology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.

Abstract

Lead (Pb) is an environmental factor suspected of contributing to neurodegenerative diseases such as Alzheimer's disease (AD). In AD, it has been postulated that increased production and/or decreased metabolism/clearance of β-amyloid (Aβ) may lead to amyloid plaque deposition as well as a cascade of other neuropathological changes. It has been suggested that Pb exposure may be associated with AD-like pathology and severe memory deficits in humans. Therefore, we investigated whether Pb exposure could induce Aβ accumulation in the brain. In this study, we demonstrated that acute Pb treatments lead to increased levels of Aβ in the cerebrospinal fluid (CSF) and brain tissues. Interestingly, Pb treatments did not affect Aβ production in brain neurons. Furthermore, Pb treatments significantly decreased LRP1 protein expression in the choroid plexus (CP). Our results suggest disrupted LRP1-mediated transport of Aβ in this region may be responsible for the Aβ accumulation in brain.

© 2010 Elsevier Ireland Ltd. All rights reserved.

PMID:
21167913
[PubMed - indexed for MEDLINE]
PMCID:
PMC3026879
Free PMC Article

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