The predominant role of GM1 deficiency became evident in work with B4galnt1-null mice that possess total ganglio-series ganglioside deficiency (including GM1), resulting in impaired movement and various neuropathological symptoms of PD, e.g., elevation and aggregation of aSyn, loss of tyrosine hydroxylase (TH)-positive dopamine (DA) neurons in the substantia nigra pars compacta (SNpc), depletion of striatal DA, and reduced pRet expression in TH+ neurons [72]. This evidence concerns the gene B4GALNT1 and Parkinson disease.