To investigate whether α-synucleinopathy confined to the vagus nerve reproduces AutD in prodromal PD, we injected AAVs containing the human mutated A53T form of the α-synuclein gene or with an empty vector into the left cervical vagus nerve of SD rats and performed gastrointestinal autonomic function assessments weekly after 1 month of injection. Interestingly, 3 months later, colonic transit time assays showed that AAV-A53T-injected rats experienced a significant increase in the time to expel the steel beads (Fig. 1A, B; Additional file 1), indicating a deficit in the colonic motility. The gene discussed is SNCA; the disease is synucleinopathy.