Let's make microglia great again in neurodegenerative disorders.

Let's make microglia great again in neurodegenerative disorders.
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DOI:
10.1007/s00702-017-1792-x
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发表时间:
2018-05
期刊:
Journal of neural transmission (Vienna, Austria : 1996)
影响因子:
--
通讯作者:
Town T
Town T
中科院分区:
其他
文献类型:
--
作者:
Guillot-Sestier MV;Town T

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所有常见的神经退行性疾病-阿尔茨海默病(AD)、帕金森病(PD)、肌萎缩性侧索硬化症(ALS)和朊病毒病(PrD)-的特征在于错误折叠的蛋白质的积累,其触发小胶质细胞(脑驻留单核吞噬细胞)的激活。这种慢性形式的神经炎症是通过患者大脑和生物流体中无数细胞因子和趋化因子的释放增加来标记的。小胶质细胞吞噬作用在疾病过程的早期受到损害,阻碍异常蛋白质的清除。本文综述了主要神经退行性疾病的免疫病理学。总体概念是,这些异常的先天免疫途径可以被靶向恢复稳态,希望诱使小胶质细胞清除神经毒性错误折叠蛋白。
All of the common neurodegenerative disorders–Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS) and prion diseases (PrD)–are characterized by accumulation of misfolded proteins that trigger activation of microglia; brain-resident mononuclear phagocytes. This chronic form of neuroinflammation is earmarked by increased release of myriad cytokines and chemokines in patient brains and biofluids. Microglial phagocytosis is compromised early in the disease process, blocking clearance of abnormal proteins. This review identifies immune pathologies shared by the major neurodegenerative disorders. The overarching concept is that these aberrant innate immune pathways can be targeted for return to homeostasis in hopes of coaxing microglia into clearing neurotoxic misfolded proteins.
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