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Infantile exposure to lead and late‐age cognitive decline: Relevance to AD
Author(s) -
Bihaqi Syed Waseem,
Bahmani Azadeh,
Subaiea Gehad M.,
Zawia Nasser H.
Publication year - 2014
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2013.02.012
Subject(s) - amyloid precursor protein , western blot , neurotoxicity , pathogenesis , cognitive decline , amyloid beta , amyloid (mycology) , alzheimer's disease , biology , disease , dementia , medicine , immunology , gene , biochemistry , toxicity , pathology
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.