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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 (Moors et al., 2019)

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Email: [email protected] Received: 16 May 2024 / Revised: 03 June 2024 / Accepted: 14 August 2024 / Published: 30 September 2024 DOI: 10.31491/APT.2024.09.148 Abstract Alzheimer's disease (AD) is a complex neurodegenerative disease and a leading cause of morbidity and mortality