Despite the growing evidence implicating GCase in neurodegenerative disorders such as PD, DLB, and GD, very little research has explored the relationship of GCase protein levels and enzyme activity to AD pathology except for the finding from Xu and colleagues suggesting that aggregates of Aβ and amyloid precursor protein (APP) are increased in GD mice, raising the possibility that GCase deficiency contributes to AD [41]. This evidence concerns the gene APP and Parkinson disease.