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. Here, GDNF is linked to Parkinsonism.