GBA1 and Parkinson disease: Furthermore, disruption of GBA in primary culture and human iPSCs leads to the accumulation of a-synuclein, in addition to Glucer acting as a stabilizer of a-synuclein, where the accumulation of a-synuclein itself inhibits GBA lysosomal function, pointing to a self-propagating feedback-loop in PD (Mazzulli et al., 2011).