As we and others have shown decreased expression of GM1 and other complex gangliosides in the SN in PD3,4 and decreased expression of genes involved in ganglioside biosynthesis in DAergic neurons in the PD SN2, it is conceivable that reduced levels of gangliosides, and particularly GM1, in the PD SN may promote the accumulation of toxic α-synuclein and that administration of GM1 may provide sufficient amounts of this important sphingolipid so as to at least partially inhibit the toxic aggregation of α-synuclein and provide some level of protection to SN DA neurons. The gene discussed is SNCA; the disease is Parkinson disease.