【摘要】 目的探讨parkin在阿尔茨海默病(AD)发病机制中的作用。方法利用经典的GAL4/UAS系统,选用nina EGAL4启动子,将突变位点在R406W处的Tau蛋白在果蝇复眼内选择性表达,构建nina E-GAL4/UAS系统AD转基因果蝇模型。然后分别在敲除和不敲除线粒体分裂蛋白Drp1情况下,使parkin在AD转基因果蝇模型中表达。结果 parkin明显抑制了AD转基因果蝇模型复眼视网膜光感受神经元变性,而在Drp1被敲除后,parkin的保护作用效果明显减弱。结论 parkin对AD转基因果蝇模型具有神经保护作用,而这种神经保护作用可能需要依赖线粒体分裂蛋白Drp1的功能。更多还原

【Abstract】 Objective To confer the influence of parkin on pathogenesis of AD.Methods Here,using the classical model of GAL4 / UAS system,and nina E-GAL4 / UAS system AD transgenic Drosophila models were constructed by using the promoter nina E-GAL4,which drive h TauR406Wprotein(Tau protein which mutation site is at R406W),selectively expression in cells of Drosophila eyes.Then,parkin protein was expressed in AD transgenic Drosophila models by genetic methods with or without in a background of mitochondrial fission protein of Drp1.Results Expression of parkin notably suppresses the neurotoxicity of retinal photoreceptors in AD transgenic Drosophila models.Moreover,RNAi knockdown of Drp1 significantly parkin’s protection against AD Drosophila.Conclusion It is confirmed that expression of parkin could protect AD transgenic Drosophila models,and the protection role of parkin is Drp1-dependent,maybe.更多还原