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The hypothesis of the gain of function in GCase theorizes that the mutant form of protein is recognized as misfolded, thus placing stress on mechanisms of protein degradation and interfering with α-synuclein breakdown and consequent endoplasmic reticulum stress, as observed in autophagy perturbations in cells derived from patients with GBA1 -associated PD ( 2.5.2 Clinical studies Monogenic PD cases due to GBA1 loss of function and subsequent substrate accumulation have been investigated in cellular and animal models and in studies of human brains of patients with GBA1 -associated PD showing to particularly affect pars compacta of SN, putamen, cerebellum, and amygdala and frontal cortex (Rocha et al., 2015)

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Using the LSL-Kras G 12 D/+ ::LSL-Trp53 R127H/+ ::Pdx-1-Cre genetic model of pancreatic cancer, administration of CDDO-Me (60 mg/kg in diet) after 4 weeks of age increased survival by about 3 weeks [400]

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