Eikelenboom P, Rozemuller J M, van Muiswinkel F L
Department of Psychiatry, Graduate School Neurosciences Amsterdam, Vrije Universiteit, Valeriuskliniek, The Netherlands.
Exp Neurol. 1998 Nov;154(1):89-98. doi: 10.1006/exnr.1998.6920.
During the past 15 years a variety of inflammatory proteins has been identified in the brains of patients with Alzheimer's disease (AD) postmortem. There is now considerable evidence that in AD the deposition of amyloid-beta (A beta) protein precedes a cascade of events that ultimately leads to a local "brain inflammatory response." Here we reviewed the evidence (i) that inflammatory mechanisms can be a part of the relevant etiological factors for AD in patients with head trauma, ischemia, and Down's syndrome; (ii) that in cerebral A beta disorders the clinical symptoms are determined to a great extent by the site of inflammation; and (iii) that a brain inflammatory response can explain some poorly understood characteristics of the clinical picture, among others the susceptibility of AD patients to delirium. The present data indicate that inflammatory processes in the brain contribute to the etiology, the pathogenesis, and the clinical expression of AD.
在过去15年中，通过对阿尔茨海默病（AD）患者进行尸检，已在其大脑中鉴定出多种炎症蛋白。现在有大量证据表明，在AD中，β-淀粉样蛋白（Aβ）的沉积先于一系列最终导致局部“脑部炎症反应”的事件。在此，我们回顾了以下证据：（i）炎症机制可能是头部创伤、缺血和唐氏综合征患者患AD的相关病因因素之一；（ii）在脑Aβ疾病中，临床症状在很大程度上取决于炎症部位；（iii）脑部炎症反应可以解释临床症状中一些难以理解的特征，尤其是AD患者易患谵妄。目前的数据表明，脑部的炎症过程与AD的病因、发病机制及临床症状均有关。
