We measured GCase enzymatic activity as well as the activity of five other lysosomal hydrolases (galactocerebrosidase (GALC, EC 3.2.1.46, deficient in Krabbe disease), alpha-glucosidase (GAA, EC 3.2.1.20, deficient in Pompe disease), alpha-galactosidase (GLA, EC 3.2.1.22, deficient in Fabry disease), sphingomyelinase (ASM, EC 3.1.4.12, deficient in Niemann–Pick disease types A and B), and alpha-iduronidase (IDUA, EC 3.2.1.76, deficient in mucopolysaccharidosis type I)) in DA neurons from the GBA-PD and GBA-carrier. This evidence concerns the gene GAA and Niemann-Pick disease type A.