This suggests that (a) depletion of GM1 ganglioside drives both α-synuclein accumulation/aggregation and GDNF resistance/Parkinsonism, and (b) α-synuclein aggregates can be eliminated by local concentrations of GDNF sufficiently high to overcome the impairment of GDNF signaling caused by GM1 ganglioside depletion. This evidence concerns the gene SNCA and Parkinson disease.