Although the underlying mechanism of how D409H expression results in increased pathologic α-synuclein aggregates at the early time point is not clear, it is likely that additional α-synuclein accumulation triggered by GBA1 deficiency due to D409H expression pushes forward the levels of α-synuclein protein to reach quickly the threshold required for pathologic α-synuclein aggregates in the model at 6 months of age, eliciting overt DA neurodegeneration loss in the SNpc and PD related motor deficits in the same model. Here, SNCA is linked to Parkinson disease.