The presence of α-synuclein inclusions, with post-translational modifications observed in the human LB, in specific brain areas of Smad3 deficient mice suggests a neuropathological status in these mice, which together with the strong DA catabolism, the loss of dopaminergic neurons and decreased trophic and astroglial support detected, may resemble early symptoms of parkinsonism in these mice. Here, SMAD3 is linked to Parkinsonism.