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神经变性中炎症的发生机制。

Mechanisms underlying inflammation in neurodegeneration.

机构信息

Department of Cellular and Molecular Medicine, University of California, San Diego, La Jolla, 92093, USA.

出版信息

Cell. 2010 Mar 19;140(6):918-34. doi: 10.1016/j.cell.2010.02.016.

Abstract

Inflammation is associated with many neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and multiple sclerosis. In this Review, we discuss inducers, sensors, transducers, and effectors of neuroinflammation that contribute to neuronal dysfunction and death. Although inducers of inflammation may be generated in a disease-specific manner, there is evidence for a remarkable convergence in the mechanisms responsible for the sensing, transduction, and amplification of inflammatory processes that result in the production of neurotoxic mediators. A major unanswered question is whether pharmacological inhibition of inflammation pathways will be able to safely reverse or slow the course of disease.

摘要

炎症与许多神经退行性疾病有关,包括阿尔茨海默病、帕金森病、肌萎缩侧索硬化症和多发性硬化症。在这篇综述中,我们讨论了导致神经炎症的诱导剂、传感器、换能器和效应器,这些因素导致神经元功能障碍和死亡。尽管炎症的诱导剂可能以疾病特异性的方式产生,但有证据表明,负责炎症过程的感应、转导和放大的机制存在显著的趋同,导致产生神经毒性介质。一个尚未解决的主要问题是,抑制炎症途径的药理学干预是否能够安全地逆转或减缓疾病的进程。

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