These results strength the possibility that γ-Syn might be a better marker of disease compared to the other synucleins, although it cannot be excluded that the lack of change in α-Syn (and β-Syn) levels in the PPN might be due to the small number of animals intoxicated with MPTP or to the rapid neurotoxic action of MPTP and the early evolution of parkinsonism it induces, in contrast to the mechanisms of long-term neurotoxicity that may take place in humans. This evidence concerns the gene SNCA and Parkinson disease.