Abstract
Cerebral amyloid β protein deposition in Alzheimer's disease is associated with a predominantly local acute phase response that kindles release of various inflammatory and immune system mediators. The molecular events are accompanied by a profound cellular response which is largely orchestrated by microglia. Current evidence suggests microglia are primarily involved in phagocytic activity and may be responsible for inducing further neuronal damage by generating reactive oxygen species and proteolytic enzymes. Antiinflammatory measures that target complement activation as well as microglial-mediated oxidative damage would provide rational therapeutic strategies.
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