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The acute-phase “panproteinase” inhibitor α 2 -macroglobulin  α 2M), 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 α 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.

α2-Macroglobulin Deletion Polymorphism and Plasma Levels in Late Onset Alzheimer's Disease