Journal
NEUROBIOLOGY OF AGING
Volume 28, Issue 8, Pages 1215-1220Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.neurobiolaging.2006.05.030
Keywords
Alzheimer's disease; late-onset Alzheimer's disease; beta-amyloid peptide; clearance; matrix metalloproteinase; genetic polymorphism; genetic association study
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Cerebral accumulation of P-amyloid peptide (A beta) is a central event in the pathogenesis of Alzheimer's disease (AD). Several proteases were shown to hydrolyze A beta in vitro or in cell-based assays, and are likely candidates for a role in A beta clearance in brain. Previous reports suggest that matrix metalloproteinases (MMPs) could be involved in such a mechanism. A functional polymorphism at position - 1171 (5A/6A) in MMP-3 was examined in two independent studies to investigate the impact of this polymorphism on the risk of developing dementia. We found that subjects APOE epsilon 4 non-carriers and 6A/6A homozygous for the MMP-3 polymorphism were at increased risk of dementia. Our findings support the hypothesis that MMPs may influence the risk of dementia. (c) 2006 Elsevier Inc. All rights reserved.
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