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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 -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 (Moors et al., 2019)

Some use liposomal delivery systems that encapsulate the peptide in lipid spheres

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The ME of PBPs can be performed in different ways, including overexpression of PPs biosynthetic structural genes and transcription factors, up and down-regulation of genes/enzymes involved in the biosynthesis of certain PPs, silencing of specific metabolic routes in phenylpropanoid pathway, down-regulation of PPs biosynthesis structural genes using interference miRNAs, and enhancing the production of intermediary substrates of phenylpropanoid enzymes (365369)

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