Glia and alpha-synuclein in neurodegeneration: A complex interaction.
Glia and alpha-synuclein in neurodegeneration: A complex interaction.
复制标题
DOI：
10.1016/j.nbd.2015.03.003
复制
发表时间：
2016-01
影响因子：
6.1
通讯作者：
Fellner L
中科院分区：
文献类型：
--
作者：
Brück D;Wenning GK;Stefanova N;Fellner L
α-突触核蛋白病（ASP）包括以α-突触核蛋白（AS）在神经元或胶质细胞中聚集为特征的成人发作的进行性神经退行性疾病，如帕金森病（PD）、路易体痴呆（DLB）和多系统萎缩（MSA）。PD和DLB的特征是神经元AS阳性包涵体，称为Lewy小体（LB），而胶质细胞胞质包涵体（GCI，Papp-Lantos小体）被认为是MSA的定义标志。此外，AS阳性细胞质聚集体也可在PD/DLB和MSA脑的星形胶质细胞中看到。胶质AS-包涵体似乎触发减少营养支持，导致神经元损失。此外，小胶质细胞增生和星形胶质细胞增生可以在整个神经退行性脑中发现，两者都是ASP启动和进展的关键参与者。在这篇综述中，我们将强调AS依赖的神经胶质功能的改变及其对神经元脆弱性的影响，从而提供了一个详细的总结，在ASP神经胶质细胞的多方面作用。
α-Synucleinopathies (ASP) comprise adult-onset, progressive neurodegenerative disorders such as Parkinson’s disease (PD), dementia with Lewy bodies (DLB) and multiple system atrophy (MSA) that are characterized by α-synuclein (AS) aggregates in neurons or glia. PD and DLB feature neuronal AS-positive inclusions termed Lewy bodies (LB) whereas glial cytoplasmic inclusions (GCIs, Papp-Lantos bodies) are recognized as the defining hallmark of MSA. Furthermore, AS-positive cytoplasmic aggregates may also be seen in astroglial cells of PD/DLB and MSA brains. The glial AS-inclusions appear to trigger reduced trophic support resulting in neuronal loss. Moreover, microgliosis and astrogliosis can be found throughout the neurodegenerative brain and both are key players in the initiation and progression of ASP. In this review, we will highlight AS-dependent alterations of glial function and their impact on neuronal vulnerability thereby providing a detailed summary on the multifaceted role of glia in ASP.