Cerebral amyloid beta protein deposition in Alzheimer's disease is ass
ociated;with a predominantly local acute phase response that kindles r
elease of various inflammatory and immune system mediators. The molecu
lar events are accompanied by a profound cellular response which is la
rgely orchestrated by microglia. Current evidence suggests microglia a
re primarily involved in phagocytic activity and may be responsible fo
r inducing further neuronal damage by generating reactive oxygen speci
es and proteolytic enzymes. Antiinflammatory measures that target comp
lement activation as well as microglial-mediated oxidative damage woul
d provide rational therapeutic strategies. (C) 1996 Academic Press Lim
ited