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.
DeFeudis
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Institute for BioScience, Grafton, MA 01519.
D000544:Alzheimer Disease / Q000188:drug therapy* / Q000378:metabolism; D000682:Amyloid / Q000378:metabolism*; D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor; D005609:Free Radicals; D006801:Humans; D011498:Protein Precursors / Q000378:metabolism*; D015842:Serine Proteinase Inhibitors / Q000627:therapeutic use*; D013482:Superoxide Dismutase / Q000627:therapeutic use*
D000682:Amyloid; D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor; D005609:Free Radicals; D011498:Protein Precursors; D015842:Serine Proteinase Inhibitors; D013482:Superoxide Dismutase