COMPLEMENT ACTIVATION IN AMYLOID PLAQUES IN ALZHEIMERS-DISEASE BRAINSDOES NOT PROCEED FURTHER THAN C3

In Alzheimer's disease (AD) patients, the complement components Clq, C 4 and C3 can be detected in different types of beta/A4 plaques, one of the hallmarks of AD. Contradictory findings on the presence of late c omplement components in AD brains have been reported. Nevertheless, it was suggested in recent studies that in AD brain complement activatio n results in complement membrane attack complex (MAC) formation and th at complement activation may, act as an intermediate between beta/A4 d eposits and the neurotoxicity observed in AD. In the present study the presence of a number of complement components and regulatory proteins in AD temporal cortex and, for comparison, in glomerulone-phritis (GN ) was analysed. In GN kidneys, besides Clq, Clr, Cls and C3, the late components and the C5b-9 complex are also associated with capillary ba sement membrane and mesangial immune complex deposits. In AD temporal cortex Clq, C3 and C3 are eo-localized with beta/A4 deposits, However: in contrast to the GN kidney, the late complement components C5, C7 a nd C9, as well as the C5b-9 membrane attack complex cannot be detected in beta/A4 positive plaques. The absence of the cytolytic C5b-9 compl ex in AD brain suggests that in AD, the complement MAC does not functi on as the proposed inflammatory mediator between beta/A4 deposits and the neurofibrillary changes.