RESUMO
Some studies have indicated that low level of anti-Abeta antibodies may play an important role in the pathogenesis of Alzheimer disease (AD), but little is known about the avidity of these antibodies. We investigated the avidity and levels of anti-Abeta antibodies in 20 AD patients and 40 healthy controls by an enzyme-linked immunosorbent assay with thiocyanate elution. Our data revealed that both the levels and the avidity of anti-Abeta antibodies were statistically lower in AD patients than in healthy controls. However, there was no correlation between both of them, suggesting that the levels and the avidity of anti-Abeta antibodies might be regulated by different mechanisms. We hypothesize that incomplete B cell immune tolerance may be the major reason for low antibody avidity in AD patients. Avidity declination in AD patients should have immunopathologic implications as antigen-antibody complexes containing low avidity antibodies are not readily cleared by the immune system.
