Linking Neuroinflammation and Neurodegeneration in Parkinson's Disease.
Linking Neuroinflammation and Neurodegeneration in Parkinson's Disease.
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DOI：
10.1155/2018/4784268
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发表时间：
2018
影响因子：
4.1
通讯作者：
Van der Perren A
中科院分区：
文献类型：
--
作者：
Gelders G;Baekelandt V;Van der Perren A
神经退行性疾病，如帕金森病（PD）和阿尔茨海默病（AD）给我们的发达和老龄化社会带来了紧迫的负担。错误折叠的蛋白质聚集体是几种神经退行性疾病的关键方面。然而，关于错误折叠的蛋白质聚集体的作用和神经元细胞死亡的原因，仍有几个问题没有答案。近年来，人们推测神经炎症过程可能在PD的发病机制中起着至关重要的作用。大量的尸检、脑成像、流行病学和动物研究都证明了先天免疫和适应性免疫参与了神经退行性变。这些炎症过程是否直接参与PD的病因学或代表黑质纹状体通路损伤的继发性后果是深入研究的主题。对细胞外α-突触核蛋白的免疫应答改变可能在调节帕金森病进展中起关键作用。在这篇综述中，我们讨论了目前的概念，神经炎症和它参与PD相关的神经退行性变。
Neurodegenerative diseases such as Parkinson's disease (PD) and Alzheimer's disease (AD) impose a pressing burden on our developed and consequently aging society. Misfolded protein aggregates are a critical aspect of several neurodegenerative diseases. Nevertheless, several questions remain unanswered regarding the role of misfolded protein aggregates and the cause of neuronal cell death. Recently, it has been postulated that neuroinflammatory processes might play a crucial role in the pathogenesis of PD. Numerous postmortem, brain imaging, epidemiological, and animal studies have documented the involvement of the innate and adaptive immunity in neurodegeneration. Whether these inflammatory processes are directly involved in the etiology of PD or represent secondary consequences of nigrostriatal pathway injury is the subject of intensive research. Immune alterations in response to extracellular α-synuclein may play a critical role in modulating Parkinson's disease progression. In this review, we address the current concept of neuroinflammation and its involvement in PD-associated neurodegeneration.
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作者：
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DOI：
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