神经药理学报

神经药理学报››2018,Vol. 8››Issue (5): 70-71.

• Session 4B: Parkinson’s and Other Neurodegenerative Diseases: Pathogenesis, Novel Treatment •上一篇下一篇

Molecular Dissection of Parkinson’s Disease

HAN Hai-long，WANG Ruo-xi，TAN Jie-qiong，ZHANG Zhuo-hua

  1. Institute of Molecular Precision Medicine，Xiangya Hospital，Central South University，Changsha，Hunan，410078，China
  • 出版日期:2018-10-26发布日期:2018-11-16
  • 通讯作者:ZHANG Zhuo-hua，E-mail: zhangzhuohua@sklmg.edu.cn

Molecular Dissection of Parkinson’s Disease

HAN Hai-long，WANG Ruo-xi，TAN Jie-qiong，ZHANG Zhuo-hua

  1. Institute of Molecular Precision Medicine，Xiangya Hospital，Central South University，Changsha，Hunan，410078，China
  • Online:2018-10-26Published:2018-11-16
  • Contact:ZHANG Zhuo-hua，E-mail: zhangzhuohua@sklmg.edu.cn

摘要：Human Genetic studies result in identification of causative genes in Parkinson’s Disease (PD). The pathophysiological function of these genes remains largely unknown. During the past decade, we focus on dissecting genetic and epigenetic controls of PD pathogenesis. In this presentation, we will focus on how PD associated genes functions in cells and animal models and their potential link to PD pathogenesis. Our studies suggest that multiple PD associated genes functionally collaborative to regulate protein and cellular organelle quality control. We also identify PD associated gene ATP13A2 as an essential component to mediate fusion of autophagosome and lysosome. However, our study indicate that autophagy participates in PD but is not essential for initiation of PD. Interestingly, mitochondrial dynamics is potentially dysregulated in the early stage of pathogenesis. Our finding opens a new direction of PD research and design of clinical diagnosis and treatment.

Abstract:Human Genetic studies result in identification of causative genes in Parkinson’s Disease (PD). The pathophysiological function of these genes remains largely unknown. During the past decade, we focus on dissecting genetic and epigenetic controls of PD pathogenesis. In this presentation, we will focus on how PD associated genes functions in cells and animal models and their potential link to PD pathogenesis. Our studies suggest that multiple PD associated genes functionally collaborative to regulate protein and cellular organelle quality control. We also identify PD associated gene ATP13A2 as an essential component to mediate fusion of autophagosome and lysosome. However, our study indicate that autophagy participates in PD but is not essential for initiation of PD. Interestingly, mitochondrial dynamics is potentially dysregulated in the early stage of pathogenesis. Our finding opens a new direction of PD research and design of clinical diagnosis and treatment.

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