报告题目：Aldehyde dehydrogenase 1 (ALDH1A1) determines the regional selectivity of nigral dopaminergic neuron loss in Parkinson’s disease
报告人：刘国祥博士（Northwestern University，Feinberg School of Medicine）
报告时间：2015年4月15日周三上午10:30
报告地点：生科院楼329会议室
报告人简介：刘国祥，男，本科毕业于浙江大学，2008年博士毕业于中科院上海生科院生化细胞所，随后分别在美国NIH-John Hopkins Univ、Northwestern University做博士后工作至今。主要从事老年化、帕金森疾病等神经退行性疾病病理方面研究。先后在Journal of Clinical Investigation，Nature Neuroscience，Neuropsychopharmarcology, Journal of Neuroscience, Human Molecular Genetics, EMBO Journal, The American Journal of Human Genetics, The Journal of Immunology等重要国际学术期刊发表文章。
报告简介：Parkinson’s disease (PD) is the most common degenerative movement disorder which affects an estimated 7million people worldwide.PD, with AD etc. neurodegenerative diseases represent some of the greatest challenges to science and medicinedue to their cost, lack of mechanism-based treatments, and the impact on individuals and caregivers. Our recent study has revealed an important mechanism underlying the pathogenesis of PD and established a potential therapeutic target. We identified a protein called aldehyde dehydrogenase 1 (ALDH1A1)as a key molecular target for preventing midbrain dopaminergic neurons from α-synuclein-induced degeneration. We generated a new line of tetracycline-regulated inducible transgenic mice that overexpressed the PD-related, mutant α-synuclein gene in the mDA neurons, and found that the mice displayed some key pathological phenotypes of PD. Furthermore, we found DA neurons can be divided into twosubpopulations based on the expression of ALDH1A1. Our findings suggest that ALDH1A1protects subpopulations of SNpc DA neurons by preventing the accumulation of dopamine aldehyde intermediatesand formation of cytotoxic α-synuclein oligomers. Hence, we propose that the activation of ALDH1A1 can delay the progress of PD, and improve the life-quality of patients.