More recently, we have shown in the MPTP/MPP+ in vivo and in vitro models of PD, respectively, that increases in α-Syn can initiate and sustain p-Tau formation with hyperphosphorylation at Ser202, Ser262 and Ser396/404, which are the same epitopes that are hyperphosphorylated in AD and lead to pathological changes [29-32]. This evidence concerns the gene MAPT and Parkinson disease.