Renato Scacchi, Maria Ruggeri, Giuseppe Gambina, Maria C. Martini, Rosa M. Corbo
?2-Macroglobulin Deletion Polymorphism and Plasma Levels in Late Onset Alzheimer's Disease
The acute-phase “panproteinase” inhibitor ?2-macroglobulin ?2M), a protein involved in inflammatory reactions, has been identified in amyloid plaques in Alzheimer's disease (AD). In addition, ?2M is involved in AD susceptibility at the genetic level, and a deletion polymorphism at the ?2M gene has been found to be associated with sporadic AD. We analyzed the deletion polymorphism and ?2M plasma levels in 93 ultraoctuagenarian patients with late-onset sporadic AD and in controls (n=157). ?2M allele frequencies did not differ between AD patients ?2M*2=0.169) and controls (?2M*2=0.146). The mean plasma concentrations of ?2M were similar in patients (271.8±79 mg/dl) and controls (269.5±81.2 mg/dl). No difference was found in the ?2M mean plasma levels associated with the three ?2M genotypes, indicating that the deletion has no effect on ?2M protein level. However, in AD patients ?2M 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 ?1-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.
Clinical Chemical Laboratory Medicine, Walter de Gruyter
Print ISSN: 1434-6621
Volume: 40, 04/2002
Pages: 333 - 336
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