炎性因子在阿尔茨海默病发病机制中的作用  

Role of inflammatory cytokines in pathogenesis of Alzheimer’ s disease

作　　者：王士博[1] 王越[1] 于晓雯[1] 杨玲[1] 龚江波[1] 拓西平[1] 

机构地区：[1]第二军医大学附属长海医院老年病科

出　　处：《中华老年多器官疾病杂志》2016年第9期713-716,共4页Chinese Journal of Multiple Organ Diseases in the Elderly

基　　金：2014年度上海市卫生和计划生育委员会科研课题重点项目(201440022)~~

摘　　要：阿尔茨海默病（ AD）是老年人中最常见的、但病因尚未明确的渐进性神经系统退行性疾病，其主要临床表现为进行性认知功能障碍、学习记忆能力减退、日常行为异常、生活能力下降以及人格改变等症状。神经元外淀粉样β蛋白（Aβ）沉积、神经元内神经原纤维缠结（ NFT）、神经突触及神经元丢失等为其主要病理学特征性变化，这些变化诱发了神经炎症反应。AD发病机制及病因复杂多样，目前主要有Aβ级联假说、tau蛋白异常磷酸化、神经炎症反应等，越来越多的研究表明炎症反应在AD发病进程中扮演重要角色。本文将对部分炎性因子[IL-1β、IL-6、IL-4、IL-10、转化生长因子β1（TGF-β1）和肿瘤坏死因子α（ TNF-α）等]与AD的关系做一综述。Alzheimer’s disease （AD） has been regarded as one of the most common neurodegenerative diseases, and is mainly manifested as progressive cognitive dysfunction, memory and learning decline, abnormal daily behavior, personality changes and decline in activities of daily living though its cause remains unclear.The main pathological features of AD have been revealed as deposition of amyloidβ-protein（ Aβ） , neurofibrillary tangles （ NFTs） , synaptic and neuronal loss etc., and these changes contribute to neurological inflammatory responses.The etiology and pathogenesis of AD are quite complex and diverse, and current most prevailing hypotheses include Aβcascade hypothesis, abnormal phosphorylation of tau protein, nerve inflammation and so on.Much evidence showed that the inflammation response played important roles in the development and progression of AD.In this paper, we reviewed the relationship of some inflammatory cytokines[IL-1β, IL-6, IL-4, IL-10, transforming growth factor-β1 （TGF-β1）, tumor necrosis factor-α（ TNF-α） and others] with AD.

关 键 词：炎性因子 阿尔茨海默病 发病机制 

分 类 号：R592[医药卫生—老年医学] R741[医药卫生—内科学]