As GD patients with the L444P mutation have pronounced cognitive deficits27, in this study, we conducted a thorough, longitudinal examination of Gba L444P mice, in conjunction with the well-established SNCA tg PD mice that overexpress mutant human α-synuclein, and their crossbreeds, i.e. Gba-SNCA mice. The gene discussed is GBA1; the disease is Parkinson disease.