Kalaria R N
CBV Path Group, MRC Unit, Newcastle General Hospital, Newcastle upon Tyne, United Kingdom.
Curr Opin Hematol. 1999 Jan;6(1):15-24. doi: 10.1097/00062752-199901000-00004.
Microglia play a major role in the cellular response associated with the pathological lesions of Alzheimer's disease. As brain-resident macrophages, microglia elaborate and operate under several guises that seem reminiscent of circulating and tissue monocytes of the leucocyte repertoire. Although microglia bear the capacity to synthesize amyloid beta, current evidence is most consistent with their phagocytic role. This largely involves the removal of cerebral amyloid and possibly the transformation of amyloid beta into fibrils. The phagocytic functions also encompass the generation of cytokines, reactive oxygen and nitrogen species, and various proteolytic enzymes, events that may exacerbate neuronal damage rather than incite outgrowth or repair mechanisms. Microglia do not appear to function as true antigen-presenting cells. However, there is circumstantial evidence that suggests functional heterogeneity within microglia. Pharmacological agents that suppress microglial activation or reduce microglial-mediated oxidative damage may prove useful strategies to slow the progression of Alzheimer's disease.
小胶质细胞在与阿尔茨海默病病理损伤相关的细胞反应中起主要作用。作为脑内常驻巨噬细胞，小胶质细胞以多种形式发挥作用，这些形式似乎让人联想到白细胞库中的循环单核细胞和组织单核细胞。尽管小胶质细胞有合成β-淀粉样蛋白的能力，但目前的证据最支持它们的吞噬作用。这主要涉及清除脑内淀粉样蛋白，并可能将β-淀粉样蛋白转化为纤维。吞噬功能还包括产生细胞因子、活性氧和氮物质以及各种蛋白水解酶，这些事件可能会加剧神经元损伤，而不是激发生长或修复机制。小胶质细胞似乎并不作为真正的抗原呈递细胞发挥作用。然而，有间接证据表明小胶质细胞内存在功能异质性。抑制小胶质细胞激活或减少小胶质细胞介导的氧化损伤的药物可能是减缓阿尔茨海默病进展的有用策略。
