DeFeudis F V
Institute for BioScience, Grafton, MA 01519.
Neurobiol Aging. 1989 Sep-Oct;10(5):467-8; discussion 477-8. doi: 10.1016/0197-4580(89)90099-7.
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.
大脑中的小胶质细胞和/或巨噬细胞通过产生氧化剂，可能在β-淀粉样前体蛋白（APP）的库尼茨蛋白酶抑制剂（KPI）结构域的局部失活中发挥作用，从而促进阿尔茨海默病（AD）患者异常淀粉样细丝的沉积。蛋白酶抑制剂和/或自由基清除剂可能作为治疗AD淀粉样变性的方法。
