For this, we utilize SNCA overexpressing cell lines, iPSC-derived dopaminergic neurons of PD patients harboring SNCA pathology (SNCA p.A53T), primary neurons and organotypic brain slices of Thy1-SNCA overexpressing mice [43, 44] as well as proof-of-concept in vivo applications in Ctsd-deficient mice exhibiting SNCA aggregation [16, 45, 46]. This evidence concerns the gene THY1 and Parkinson disease.