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Experimental models of Parkinson's disease.

机译:帕金森氏病的实验模型。

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Research into the pathogenesis of Parkinson's disease has been rapidly advanced by the development of animal models. Initial models were developed by using toxins that specifically targeted dopamine neurons, the most successful of which used 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, a toxin that causes parkinsonism in man. More recently, the identification of alpha-synuclein mutations as a rare cause of Parkinson's disease has led to the development of alpha-synuclein transgenic mice and Drosophila. Here, I discuss the merits and limitations of these different animal models in our attempts to understand the physiology of Parkinson's disease and to develop new therapies.
机译:通过动物模型的发展,对帕金森氏病发病机理的研究已迅速推进。通过使用专门针对多巴胺神经元的毒素开发了最初的模型,其中最成功的毒素是使用1-甲基-4-苯基-1,2,3,6-四氢吡啶,这种毒素会导致人的帕金森氏症。最近,鉴定出α-突触核蛋白突变是帕金森氏病的罕见原因,导致了α-突触核蛋白转基因小鼠和果蝇的发展。在这里,我将讨论这些不同动物模型的优缺点,以试图了解帕金森氏病的生理学并开发新的疗法。

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