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Parkin mediates beclin-dependent autophagic clearance of defective mitochondria and ubiquitinated Abeta in AD models.Parkin 通过自噬作用介导 AD 模型中缺陷线粒体和泛素化 Abeta 的清除。
Hum Mol Genet. 2011 Jun 1;20(11):2091-102. doi: 10.1093/hmg/ddr091. Epub 2011 Mar 4.
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Regulation of tau pathology by the microglial fractalkine receptor.小胶质细胞 fractalkine 受体对 tau 病理学的调节。
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CX3CR1 deficiency alters microglial activation and reduces beta-amyloid deposition in two Alzheimer's disease mouse models.CX3CR1 缺失改变小胶质细胞激活并减少两种阿尔茨海默病小鼠模型中的 β-淀粉样蛋白沉积。
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Microglial Cx3cr1 knockout prevents neuron loss in a mouse model of Alzheimer's disease.小胶质细胞 Cx3cr1 基因敲除可预防阿尔茨海默病小鼠模型中的神经元丢失。
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Nonresolving inflammation.未解决的炎症。
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The inflammasomes.炎症小体。
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Pattern recognition receptors and inflammation.模式识别受体与炎症。
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Regulatory T cells attenuate Th17 cell-mediated nigrostriatal dopaminergic neurodegeneration in a model of Parkinson's disease.调节性 T 细胞可减轻帕金森病模型中 Th17 细胞介导的黑质纹状体多巴胺能神经退行性变。
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神经退行性病变早期的炎症反应。

Inflammation in the early stages of neurodegenerative pathology.

机构信息

Department of Neuroscience, Georgetown University Medical Center, Washington, DC 20007, USA.

出版信息

J Neuroimmunol. 2011 Sep 15;238(1-2):1-11. doi: 10.1016/j.jneuroim.2011.07.002. Epub 2011 Aug 5.

DOI:10.1016/j.jneuroim.2011.07.002
PMID:21820744
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3176984/
Abstract

Inflammation is secondary to protein accumulation in neurodegenerative diseases, including Alzheimer's, Parkinson's and Amyotrophic Lateral Sclerosis. Emerging evidence indicate sustained inflammatory responses, involving microglia and astrocytes in animal models of neurodegeneration. It is unknown whether inflammation is beneficial or detrimental to disease progression and how inflammatory responses are induced within the CNS. Persistence of an inflammatory stimulus or failure to resolve sustained inflammation can result in pathology, thus, mechanisms that counteract inflammation are indispensable. Here we review studies on inflammation mediated by innate and adaptive immunity in the early stages of neurodegeneration and highlight important areas for future investigation.

摘要

在神经退行性疾病中,包括阿尔茨海默病、帕金森病和肌萎缩侧索硬化症,炎症是由蛋白质积累引起的。新出现的证据表明,在神经退行性变的动物模型中,持续的炎症反应涉及小胶质细胞和星形胶质细胞。目前尚不清楚炎症对疾病进展是有益还是有害,以及炎症反应是如何在中枢神经系统中引发的。炎症刺激的持续存在或未能解决持续的炎症可能导致病理学,因此,对抗炎症的机制是不可或缺的。在这里,我们回顾了神经退行性疾病早期阶段由先天和适应性免疫介导的炎症研究,并强调了未来研究的重要领域。