Eikelenboom P, Veerhuis R
Graduate School Neurosciences Amsterdam, Research Institute Neurosciences Vrije Universiteit, Department of Psychiatry, Amsterdam, The Netherlands.
Neurobiol Aging. 1996 Sep-Oct;17(5):673-80. doi: 10.1016/0197-4580(96)00108-x.
A variety of inflammatory mediators including complement activation products, protease inhibitors, and cytokines are colocalized with beta-amyloid (A beta) deposits in the Alzeimer's disease (AD) brain. Activation products of the early complement components C1, C4, and C3 are always found in neuritic plaques and to a lesser extent in varying numbers of diffuse plaques. In contrast to these findings, no immunohistochemical evidence was obtained for the presence of the late complement components C7 and C9 and the complement membrane attack complex in the neuropathological lesions in AD brains. The mRNA encoding the late complement components C7 and C9 appears to be hardly or not detectable. These findings indicate that in AD the complement system does not act as an inflammatory mediator through membrane attack complex formation, but through the actions of the early complement products. In this review we focus on the role of complement in the pathological amyloid cascade in AD. In our opinion, the early complement activation products play a crucial role as mediators between the A beta deposits and the inflammatory responses leading to neurotoxicity.
包括补体激活产物、蛋白酶抑制剂和细胞因子在内的多种炎症介质与阿尔茨海默病（AD）脑内的β-淀粉样蛋白（Aβ）沉积物共定位。早期补体成分C1、C4和C3的激活产物总是存在于神经炎性斑块中，在数量不等的弥漫性斑块中含量较少。与这些发现相反，在AD脑的神经病理病变中，未获得晚期补体成分C7和C9以及补体膜攻击复合物存在的免疫组织化学证据。编码晚期补体成分C7和C9的mRNA似乎很难检测到或根本无法检测到。这些发现表明，在AD中，补体系统并非通过膜攻击复合物的形成来充当炎症介质，而是通过早期补体产物的作用来发挥作用。在本综述中，我们重点关注补体在AD病理淀粉样蛋白级联反应中的作用。我们认为，早期补体激活产物作为Aβ沉积物与导致神经毒性的炎症反应之间的介质发挥着关键作用。
