In α-synuclein aggregate rodent models of PD, overexpression of GBA1 has been demonstrated to have a neuroprotective effect by reducing oligomeric and aggregated forms of α-synuclein, restoring autophagy and lysosomal pathways, as well as preventing α-synuclein-mediated degeneration of dopamine neurons [30–33]. Here, GBA1 is linked to Parkinson disease.