Low alpha-synuclein 126 mRNA levels in dementia with Lewy bodies and Alzheimer disease
Low alpha-synuclein 126 mRNA levels in dementia with Lewy bodies and Alzheimer disease
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DOI：
10.1097/01.wnr.0000224773.66904.e7
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发表时间：
2006-08-21
期刊：
影响因子：
1.7
通讯作者：
Ariza, Aurelio
中科院分区：
文献类型：
--
作者：
Beyer, Katrin;Humbert, Jordi;Ariza, Aurelio
α-突触核蛋白是突触核蛋白病和阿尔茨海默病老年斑中路易体的主要成分，主要参与神经变性。迄今为止，已经描述了由选择性剪接产生的三种不同的亚型（α-突触核蛋白112、126和140）。本研究探讨了 6 名路易体痴呆患者、8 名路易体变异型阿尔茨海默病患者、8 名阿尔茨海默病患者和 10 名对照者前额皮质中 α-突触核蛋白 126 mRNA 的表达水平。相对 α-突触核蛋白 126 表达水平通过实时聚合酶链反应和竞争体技术测定。与对照组相比，三种痴呆症患者的 α-突触核蛋白 126 mRNA 表达显着降低，表明这种 α-突触核蛋白异构体在正常大脑中发挥着重要作用。
Alpha-synuclein, a main component of Lewy bodies in synucleinopathies and senile plaques in Alzheimer disease, is centrally involved in neurodegeneration. Three different isoforms (alpha-synuclein 112, 126, and 140) resulting from alternative splicing have been described so far. The present study explores alpha-synuclein 126 mRNA expression levels in the prefrontal cortex of six patients with dementia with Lewy bodies, eight patients with Lewy body variant of Alzheimer disease, eight patients with Alzheimer disease, and 10 controls. Relative alpha-synuclein 126 expression levels were determined by real-time polymerase chain reaction with competimer technology. Alpha-synuclein 126 mRNA expression was markedly decreased in the three dementias in comparison with controls, suggesting an important role of this alpha-synuclein isoform in the normal brain.