
pmid: 16822591
Cerebral accumulation of beta-amyloid peptide (Abeta) is a central event in the pathogenesis of Alzheimer's disease (AD). Several proteases were shown to hydrolyze Abeta in vitro or in cell-based assays, and are likely candidates for a role in Abeta 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 epsilon4 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.
Aged, 80 and over, Male, Risk, Polymorphism, Genetic, Apolipoprotein E4, DNA Mutational Analysis, Gene Frequency, Alzheimer Disease, Humans, Dementia, Female, Matrix Metalloproteinase 3, Alleles, Aged, Retrospective Studies
Aged, 80 and over, Male, Risk, Polymorphism, Genetic, Apolipoprotein E4, DNA Mutational Analysis, Gene Frequency, Alzheimer Disease, Humans, Dementia, Female, Matrix Metalloproteinase 3, Alleles, Aged, Retrospective Studies
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