GBA1 and Gaucher disease: It should be noted that in this report and those described in this section (39, 44) the CBE concentration used for in vitro experiments inhibited GCase activity by >90%, and are therefore more likely to be modelling Gaucher disease, rather than PD with heterozygote GBA mutations, where 40–60% loss of GCase activity has been reported in post-mortem brains (6, 9).