Novel therapy for Alzheimer's disease.

Recent results support the hypothesis that microglia and/or macrophages of the brain, by producing oxidants, could play a role in the local inactivation of the Kunitz protease inhibitor (KPI) domain of beta-amyloid precursor protein (APP), thereby facilitating deposition of abnormal amyloid filaments in patients with Alzheimer's disease (AD). Protease inhibitors and/or free radical scavengers might serve as therapy for the amyloidosis of AD.