Kalaria R N, Cohen D L, Premkumar D R
Department of Neurology, Neurosciences and Pathology, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA.
Neurodegeneration. 1996 Dec;5(4):497-503. doi: 10.1006/neur.1996.0069.
Cerebral amyloid beta 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.
阿尔茨海默病中脑淀粉样β蛋白沉积与主要的局部急性期反应相关，该反应引发各种炎症和免疫系统介质的释放。这些分子事件伴随着由小胶质细胞在很大程度上精心协调的深刻细胞反应。目前的证据表明，小胶质细胞主要参与吞噬活动，并可能通过产生活性氧和蛋白水解酶导致进一步的神经元损伤。针对补体激活以及小胶质细胞介导的氧化损伤的抗炎措施将提供合理的治疗策略。
