To explore how GBA1 mutations lead to neurodegeneration in GD, PD and DLB, we developed a novel invertebrate model of GBA1 insufficiency by deleting the Drosophila GBA1 homolog, dGBA1b. We found that dGBA1b mutants have multiple phenotypes consistent with neuronal dysfunction as seen in PD, DLB and GD, and dramatically increased protein aggregation that is normally cleared through an autophagic mechanism. This evidence concerns the gene GBA1 and Parkinson disease.