Interestingly, Based on the above evidence, we hypothesize that the decrease of GRASP65 in DA neurons of PD may lead to the fragmentation and abnormal function of Golgi, which in turn affects the defective glycosylation modification of DAT and its transport to the membrane. In our study, a reduction in GRASP65 was observed in both PFC and VTA of PD mice as well as PD cells, which can be reversed by GDNF; moreover, GDNF alleviated Golgi fragmentation and reduced the accumulation of non-glycosylated DAT in the Golgi on PD cells. This evidence concerns the gene GDNF and Parkinson disease.