Clinical PD begins as an axonopathy in which striatal terminal depletion and subsequent neurotransmittive failure provokes phenotypic onset.37–39 One of the α-syn’s primary roles in striatal axonopathy is phenotypic insult through synaptic injury.37–41 To that end, our model represents early PD-like pathology in which striatal innervation loss can clearly be observed through reductions in TH and DAT immunoreactive densities and depleted levels of striatal dopamine (Fig. 3). This evidence concerns the gene SLC6A3 and Parkinson disease.