GBA1 and Parkinson disease: In animal models of disease, decreased GCase activity results in increased CNS α‐synuclein/ubiquitin/tau aggregates and associated cognitive and motor deficits.73 These pathological and behavioral aberrations can be ameliorated (and even reversed) by viral gene therapy‐mediated overexpression of exogenous GCase in the CNS, which would act by restoring membrane glycosphingolipid balance (Fig. 1).73, 74, 75 These studies provide strong support for GBA augmentation as a therapy for GBA‐associated PD and conceivably for certain forms of sporadic PD disease.