Document Detail


Environmental risk factors and the developmental basis for Alzheimer's disease.
MedLine Citation:
PMID:  16519009     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Alzheimer's disease (AD) is a progressive neurodegenerative disorder whose clinical manifestations appear in old age. The hallmark pathological features of AD (amyloid plaques and associated proteins) are present in normal aging indivduals, suggesting that AD may result from the acceleration of normal age-related processes in the brain. The sporadic nature of most AD cases strongly argues for an environmental link that may drive AD pathogenesis; however, it is unclear when this environmental stress may occur. Therefore it is important to identify an environmental trigger(s) and to pinpoint the period during which such factors pose the greatest risk. Recently, we reported that developmental exposure of rats to the xenobiotic metal lead (Pb) resulted in a delayed overexpression (20 months later) of the amyloid precursor protein (APP) and its amyloidogenic Abeta product. Similarly, aged monkeys exposed to Pb as infants also responded in the same way. These data suggest that environmental influences occurring during brain development predetermine the expression and regulation of APP later in life, potentially influencing the course of amyloidogenesis, and argue for both an environmental trigger and a developmental origin of AD. In this review, we present evidence for the developmental basis of neurodegeneration and discuss mechanisms that may explain how perturbations during development can have long-term or delayed consequences in the aging brain.
Authors:
Nasser H Zawia; M Riyaz Basha
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review    
Journal Detail:
Title:  Reviews in the neurosciences     Volume:  16     ISSN:  0334-1763     ISO Abbreviation:  Rev Neurosci     Publication Date:  2005  
Date Detail:
Created Date:  2006-03-07     Completed Date:  2006-03-27     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  8711016     Medline TA:  Rev Neurosci     Country:  England    
Other Details:
Languages:  eng     Pagination:  325-37     Citation Subset:  IM    
Affiliation:
Neurotoxicology and Epigenomics Lab, Department of Biomedical and Pharmaceutical Sciences, University of Rhode Island, Kingston 02881, USA. nzawia@uri.edu
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MeSH Terms
Descriptor/Qualifier:
Age of Onset
Alzheimer Disease / etiology*,  pathology,  physiopathology*
Amyloid beta-Protein Precursor / genetics,  metabolism
Animals
Brain / drug effects,  growth & development,  pathology
Environment*
Epigenesis, Genetic
Gene Expression Regulation / drug effects
Humans
Lead / toxicity
Promoter Regions, Genetic
Risk Factors
Grant Support
ID/Acronym/Agency:
ES013022/ES/NIEHS NIH HHS; ES08104/ES/NIEHS NIH HHS
Chemical
Reg. No./Substance:
0/Amyloid beta-Protein Precursor; 7439-92-1/Lead

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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