THY1 and Parkinson disease: Conversely, several studies have been performed on transgenic mice overexpressing human wild-type α-synuclein (Thy1-αSyn), which reproduced key features of Parkinson’s disease in the absence of GCase mutations, including nonmotor deficits, pathological, biochemical, and molecular alterations, and at older ages, alterations in nigrostriatal dopaminergic neurons, including loss of striatal dopamine (PD models) [101,102].