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多系统萎缩的体外模型

In vitro models of multiple system atrophy.

作者信息

Stefanova Nadia, Reindl Markus, Poewe Werner, Wenning Gregor K

机构信息

Neurological Research Laboratory, Department of Neurology, University Hospital of Innsbruck, Austria.

出版信息

Mov Disord. 2005 Aug;20 Suppl 12:S53-6. doi: 10.1002/mds.20540.

Abstract

alpha-Synuclein represents the major constituent of oligodendroglial cytoplasmic inclusions, the hallmark lesion of multiple system atrophy (MSA), a progressive disorder that is associated with selective degenerative cell loss in basal ganglia, cerebellum, brainstem, and spinal cord. The role of abnormal alpha-synuclein aggregation in oligodendroglial cells is still obscure, in particular, whether alpha-synuclein might impair oligodendroglial and, secondarily, neuronal integrity of those cells in the diseased brain. In an attempt to answer some of these questions, we have developed an "in vitro model of MSA" by expressing the wild-type or C-terminally truncated form of alpha-synuclein in glial cell cultures. With this simplified system, we have demonstrated that alpha-synuclein significantly affects the survival of glia and its vulnerability to environmental stress, which might represent a major step in the pathogenesis of MSA.

摘要

α-突触核蛋白是少突胶质细胞质内含物的主要成分,少突胶质细胞质内含物是多系统萎缩(MSA)的标志性病变,MSA是一种进行性疾病,与基底神经节、小脑、脑干和脊髓中的选择性退行性细胞丢失有关。α-突触核蛋白在少突胶质细胞中异常聚集的作用仍不清楚,特别是α-突触核蛋白是否可能损害少突胶质细胞,进而损害患病大脑中这些细胞的神经元完整性。为了回答其中一些问题,我们通过在胶质细胞培养物中表达野生型或C末端截短形式的α-突触核蛋白,建立了一个“MSA体外模型”。利用这个简化系统,我们证明了α-突触核蛋白显著影响胶质细胞的存活及其对环境应激的易感性,这可能是MSA发病机制中的一个主要步骤。

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