In spite of the huge progress in pathogenic modeling using a range of toxins and transgenic, knockout, viral-based models of gene defects in familial PD (FPD) and mutant rodents, none of the existing PD animal models recapitulate most key features of the disease, namely derangements in DAergic synaptic transmission, selective neurodegeneration, neurochemical deficits, α-synuclein-positive neuropathology, involvement of extra-nigral areas, the motor and non-motor deficits, and drug responsiveness as seen in humans (Jenner 2008; Manning-Bog and Langston 2007). Here, SNCA is linked to Parkinson disease.