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Alzheimers Dement. 2014 Mar;10(2):187-95. doi: 10.1016/j.jalz.2013.02.012. Epub 2013 Jul 15.

Infantile exposure to lead and late-age cognitive decline: relevance to AD.

Author information

1
Department of Biomedical and Pharmaceutical Sciences, University of Rhode Island, Kingston, RI, USA.
2
Interdisciplinary Neuroscience Program (INP), University of Rhode Island, Kingston, RI, USA.
3
Department of Biomedical and Pharmaceutical Sciences, University of Rhode Island, Kingston, RI, USA; Interdisciplinary Neuroscience Program (INP), University of Rhode Island, Kingston, RI, USA. Electronic address: nzawia@uri.edu.

Abstract

BACKGROUND:

Early-life lead (Pb) exposure induces overexpression of the amyloid beta precursor protein and its amyloid beta product in older rats and primates. We exposed rodents to Pb during different life span periods and examined cognitive function in old age and its impact on biomarkers associated with Alzheimer's disease (AD).

METHODS:

Morris, Y, and the elevated plus mazes were used. Western blot, quantitative polymerase chain reaction (qPCR), and enzyme-linked immunosorbent assay were used to study the levels of AD biomarkers.

RESULTS:

Cognitive impairment was observed in mice exposed as infants but not as adults. Overexpression of AD-related genes (amyloid beta precursor protein and β-site amyloid precursor protein cleaving enzyme 1) and their products, as well as their transcriptional regulator-specificity protein 1 (Sp1)-occurred only in older mice with developmental exposure to Pb.

CONCLUSIONS:

A window of vulnerability to Pb neurotoxicity exists in the developing brain that can influence AD pathogenesis and cognitive decline in old age.

KEYWORDS:

Aging; Alzheimer's disease; Cognition; Development; Lead; Life span

PMID:
23867794
PMCID:
PMC3864613
DOI:
10.1016/j.jalz.2013.02.012
[Indexed for MEDLINE]
Free PMC Article
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