PMID: 2510040Sep 1, 1989Paper

Novel therapy for Alzheimer's disease

Neurobiology of Aging
F V DeFeudis

Abstract

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.

References

Sep 1, 1989·Neurobiology of Aging·C B Caputo, A I Salama

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Citations

Jun 1, 1993·The British Journal of Psychiatry : the Journal of Mental Science·M J Dickinson, I Singh

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