Rifampicin reduces &agr;-synuclein in a transgenic mouse model of multiple system atrophy
Rifampicin reduces &agr;-synuclein in a transgenic mouse model of multiple system atrophy
复制标题
利福平可减少
作者：
K. Ubhi;E. Rockenstein;M. Mante;C. Patrick;A. Adame;Monica Thukral;C. Shults;E. Masliah
多系统萎缩(MSA)是一种进行性神经退行性疾病，其特征是少树突状细胞胞浆内包涵体含有异常聚集的突触核蛋白。这种聚集与MSA中观察到的神经变性有关。目前的MSA治疗旨在控制症状，而不是解决神经变性的根本原因。本研究在MSA转基因小鼠模型中研究了抗生素利福平减少突触核蛋白聚集和相关神经变性的能力。我们报告，在利福平治疗后，单体和寡聚-agr；-突触核蛋白减少，磷酸化&agr；-突触核蛋白减少(S129)。这种-agr；-突触核蛋白聚集性的减少伴随着神经退变的减少。根据利福平的抗聚集特性，我们得出结论，利福平可能对MSA具有治疗潜力。
Multiple system atrophy (MSA) is a progressive neurodegenerative disorder characterized by oligodendrocytic cytoplasmic inclusions containing abnormally aggregated &agr;-synuclein. This aggregation has been linked to the neurodegeneration observed in MSA. Current MSA treatments are aimed at controlling symptoms rather than tackling the underlying cause of neurodegeneration. This study investigates the ability of the antibiotic rifampicin to reduce &agr;-synuclein aggregation and the associated neurodegeneration in a transgenic mouse model of MSA. We report a reduction in monomeric and oligomeric &agr;-synuclein and a reduction in phosphorylated &agr;-synuclein (S129) upon rifampicin treatment. This reduction in &agr;-synuclein aggregation was accompanied by reduced neurodegeneration. On the basis of its anti-aggregenic properties, we conclude that rifampicin may have therapeutic potential for MSA.
DOI：
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发表时间：
2000
期刊：
The American journal of pathology
影响因子：
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作者：
L. Hsu;Y. Sagara;A. Arroyo;E. Rockenstein;A. Sisk;M. Mallory;J. Wong;T. Takenouchi;M. Hashimoto-M.
通讯作者：
L. Hsu;Y. Sagara;A. Arroyo;E. Rockenstein;A. Sisk;M. Mallory;J. Wong;T. Takenouchi;M. Hashimoto-M.