Huntingtons disease (HD) is a neurodegenerative disorder characterized by a triad of symptoms,including involuntary choreiform movements,psychiatric disturbance,cognitive impairment and behavioral abnormalities.HD is caused by an expansion of a trinucleotide (CAG) repeat encoding a polyglutamine tract in the N terminal of huntingtin (Htt).A neuropathological hallmark in human HD and mouse models is the intracellular accumulation and aggregation of N-terminal Htt fragments,suggesting that aberrant Htt proteolysis and/or dysfunctional clearance of Htt fragments may underlie the neuropathology in HD.Htt is cleaved by caspase3 in vivo at the caspase consensus sites at amino acid 552 and 586.To enhance transfection rate of htt,we constructed an adenovirus expression system.We expressed wild-type htt552-18Q and mutant htt552-100Q in PC12 cells with adenovirus-Htt-18Q-552aa and adenovirus-100Q-552 aa.The adenovirus-null was used as a control.The activation of autophagy was assessed with Monodansylcadaverine (MDC) staining.