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阿尔茨海默病和帕金森病中的炎症过程:细胞因子的核心作用

Inflammatory Process in Alzheimer's and Parkinson's Diseases: Central Role of Cytokines.

作者信息

Alam Qamre, Alam Mohammad Zubair, Mushtaq Gohar, Damanhouri Ghazi A, Rasool Mahmood, Kamal Mohammad Amjad, Haque Absarul

机构信息

King Fahd Medical Research Center, King Abdulaziz University, P. O. Box 80216, Jeddah, Saudi Arabia.

出版信息

Curr Pharm Des. 2016;22(5):541-8. doi: 10.2174/1381612822666151125000300.

DOI:10.2174/1381612822666151125000300
PMID:26601965
Abstract

Alzheimer's disease (AD) and Parkinson's disease (PD) are the two most widespread neurological disorders (NDs) characterized by degeneration of cognitive and motor functions due to malfunction and loss of neurons in the central nervous system (CNS). Numerous evidences have established the role of neuroinflammation in the AD and PD pathology. The inflammatory components such as microglia, astrocytes, complement system and cytokines are linked to neuroinflammation in the CNS. More specifically, cytokines have been found to play a central role in the neuroinflammation of AD and PD. A number of studies have demonstrated abnormally elevated levels of inflammatory cytokines such as interleukin-1β (IL-1β) and tumor necrosis factor (TNF) in AD and PD patients. Activated microglial cells have been shown to be involved in the secretion of pro-inflammatory cytokines such as IL-1, IL-6, TNF-α and transforming growth factor-β, thereby contributing towards the progress of NDs. In addition, studies on AD pathogenesis have demonstrated that microglia produce beta-amyloid protein (Aβ), which by itself is pro-inflammatory and causes activation of several inflammatory components. Similarly, chronic inflammation caused by microglial cells is the fundamental process involved in the destruction of neurons associated with dopamine (DA)-production in the brain of PD patients. Hence, there is a need to explore the key inflammatory components in AD and PD pathogenesis in order to fully understand the root cause and establish a substantial link between these two disorders. Such knowledge will help in better management and treatment of AD and PD.

摘要

阿尔茨海默病(AD)和帕金森病(PD)是两种最常见的神经退行性疾病,其特征是由于中枢神经系统(CNS)中神经元功能异常和丧失导致认知和运动功能退化。大量证据表明神经炎症在AD和PD病理过程中发挥作用。炎症成分如小胶质细胞、星形胶质细胞、补体系统和细胞因子与CNS中的神经炎症相关。更具体地说,细胞因子已被发现在AD和PD的神经炎症中起核心作用。多项研究表明,AD和PD患者体内炎症细胞因子如白细胞介素-1β(IL-1β)和肿瘤坏死因子(TNF)水平异常升高。活化的小胶质细胞已被证明参与促炎细胞因子如IL-1、IL-6、TNF-α和转化生长因子-β的分泌,从而促进神经退行性疾病的进展。此外,关于AD发病机制的研究表明,小胶质细胞产生β-淀粉样蛋白(Aβ),其本身具有促炎作用,并导致多种炎症成分的激活。同样,小胶质细胞引起的慢性炎症是PD患者大脑中与多巴胺(DA)生成相关的神经元破坏所涉及的基本过程。因此,有必要探索AD和PD发病机制中的关键炎症成分,以便充分了解其根本原因,并在这两种疾病之间建立实质性联系。这些知识将有助于更好地管理和治疗AD和PD。

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