线粒体功能障碍与帕金森病（PD）的发生、发展有密切关系，PGC-1α为线粒体合成的主调控基因，近年来普遍认为PGC-1α有可能成为早期干预PD的重要治疗靶点，但在PD的发病机制中PGC-1α信号转导对线粒体生物活性影响的具体机制尚不明确。本研究选用SH-SY5Y细胞体系以及健康雄性C57BL小鼠建立PD的细胞以及动物模型，通过分子克隆技术、目标蛋白过表达、RNA干扰、免疫荧光、激光共聚焦等技术，对在PD发病机制中PGC-1α信号转导与线粒体生物活性之间的关系进行系统探讨，以全面了解这一过程（PGC-1α的核转位、转录激活等）及其分子机制。该研究结果将明确PGC-1α在PD中对多巴胺能神经元线粒体功能影响的具体调控机制，为PD的未来防治靶点提供新的思路。

The mitochondrial dysfunction is associated with Parkinson disease (PD). In recent years,PGC-1α, the master regulatory genes of mitochondrial synthesis, generally t may be an important therapeutic target for early intervention of PD. However, the specific mechanisms of PGC-1α signal transduction in mitochondria biological activity is not clear. In this study the SH-SY5Y cell system and male C57BL mice will be used to set up the PD models. The techniques of molecular cloning, the target protein overexpression, RNA interference, immunofluorescence and confocal laser technology will be used to systematically explore the relationship between PGC-1α signal transduction and mitochondrial biogenesis. PGC-1α nuclear translocation, transcriptional activation and its molecular mechanism will be elucidated. The study results will identify the adjustment mechanism of PGC-1α on mitochondrial function in PD, and provide new ideas for future prevention and treatment targets in PD.