GBA1 and Parkinson disease: The accumulation of GlcCer or glucosylsphingosine (GlcSph; deacetylated GlcCer) could contribute to lysosomal dysfunction and toxicity, and so to the pathogenesis of PD in GBA1 mutation carriers.13, 14 However, although PD+GBA brains have significant loss of GCase activity, the residual function of the enzyme may be sufficient to prevent substrate accumulation.