Following these seminal data, we investigated the issue throughout the brain of MPTP-intoxicated macaques looking at α-synuclein, tau, gliosis (Vital et al. 2010). Our data revealed a widespread immunoreactivity for both α-synuclein and tau in several brain regions of the MPTP-lesioned macaques. These included the substantia nigra, pons, medulla oblongata and cerebellum (dentate nucleus). GFAP staining was marked in the substantia nigra and pallidum. Interestingly, although the tauopathy was not corrected by the levodopa treatment, the immunostaining for α-synuclein was clearly reduced in the pallidum, pons, medulla oblongata, and cerebellum but not in the substantia nigra (Vital et al. 2010). This study extends the validity of the MPTP-lesioned macaque model of PD to pathological findings. In addition, it suggests that while α-synuclein increased expression is levodopa-insensitive in the substantia nigra, it is sensitive to dopamine replacement therapy in other brain regions. These data therefore offer a window for studying dopamine/synuclein interactions and their consequences on widespread neurodegeneration.