α2-Macroglobulin Deletion Polymorphism and Plasma Levels in Late Onset Alzheimer's Disease
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Renato Scacchi
Abstract
The acute-phase “panproteinase” inhibitor α2-macroglobulin α2M), a protein involved in inflammatory reactions, has been identified in amyloid plaques in Alzheimer's disease (AD). In addition, α2M is involved in AD susceptibility at the genetic level, and a deletion polymorphism at the α2M gene has been found to be associated with sporadic AD. We analyzed the deletion polymorphism and α2M plasma levels in 93 ultraoctuagenarian patients with late-onset sporadic AD and in controls (n=157). α2M allele frequencies did not differ between AD patients α2M*2=0.169) and controls (α2M*2=0.146). The mean plasma concentrations of α2M were similar in patients (271.8±79 mg/dl) and controls (269.5±81.2 mg/dl). No difference was found in the α2M mean plasma levels associated with the three α2M genotypes, indicating that the deletion has no effect on α2M protein level. However, in AD patients α2M mean plasma values differed significantly according to apolipoprotein E genotypes (p=0.03), with E3/E3 homozygotes showing the highest levels. Since in a previous work E3/E3 were found to be associated with the highest plasma levels of α1-antichymotrypsin, another acute-phase protein, the present findings seem to support the hypothesis that inflammation may be a relevant factor in AD pathogenesis peculiar to E3/E3 subjects.
Copyright © 2002 by Walter de Gruyter GmbH & Co. KG
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