A pathogenic relevance of defective autophagy promoting α-syn aggregation in PD is also supported by the studies in cellular and animal models overexpressing PD-associated mutations in the leucine-rich repeat serine/threonine-protein kinase 2 (LRRK2) [244], vacuolar protein sorting-associated protein 35 (VPS35) [245] and showing putative interactions of parkin with mutant glucocerebrosidase [246]. Here, GBA1 is linked to Parkinson disease.