SNCA and Parkinsonism: Although the exact mechanism by which GBA1 mutations increase Parkinson's risk is still unknown, it is likely that, as in idiopathic Parkinson’s disease, accumulation of alpha-synuclein, autophagic and lysosomal dysfunction, mitochondrial impairment, and oxidative and endoplasmic reticulum stress may all contribute to the development and progression of Parkinson-GBA1 (Schapira and Tolosa, 2010; Sato et al., 2013; Migdalska-Richards and Schapira, 2016).