GBA1 and Parkinson disease: Abnormal mitochondrial morphology and function, increased ROS, reduced ATP production, autophagosome accumulation, and impaired mitophagy have been observed in GBA1 L444P heterozygous mutant mouse models, GBA1 knockout mice, and GCase-deficient Drosophila brains, findings that are consistent with those observed in patients with GBA1-PD [186, 196–198].