The presence of a redistribution and size change of DAT/α-synuclein complexes in the caudate putamen of PD, when coupled to the results of our studies on experimental models showing that α-synuclein aggregation impairs DAT function by inducing its translocation from the plasma membrane to intracellular DAT/α-synuclein-positive inclusions [7,10], supports that the resulting impairment of DA turnover at dopaminergic synapses could play a pathological role in the early phases of α-synuclein deposition at striatal terminals in PD. Here, SNCA is linked to Parkinson disease.