Glucocerebrosidase deficits in sporadic Parkinson disease
Copyright policy )Glucocerebrosidase deficits in sporadic Parkinson disease
Parkinson disease (PD) is a progressive neurodegenerative movement disorder characterized pathologically by abnormal SNCA/α-synuclein protein inclusions in neurons. Impaired lysosomal autophagic degradation of cellular proteins is implicated in PD pathogenesis and progression. Heterozygous GBA mutations, encoding lysosomal GBA/glucocerebrosidase (glucosidase, β, acid), are the greatest genetic risk factor for PD, and reduced GBA and SNCA accumulation are related in PD models. Here we review our recent human brain tissue study demonstrating that GBA deficits in sporadic PD are related to the early accumulation of SNCA, and dysregulation of chaperone-mediated autophagy (CMA) pathways and lipid metabolism.
- UNSW Sydney Australia
- Neuroscience Research Australia Australia
autophagy, glucocerebrosidase, 610, Parkinson Disease, Lipid Metabolism, Parkinson disease, α-synuclein, lysosomes, 616, chaperonemediated autophagy, Autophagy, alpha-Synuclein, Glucosylceramidase, Humans, ceramide, anzsrc-for: 110903 Central Nervous System, Molecular Chaperones
autophagy, glucocerebrosidase, 610, Parkinson Disease, Lipid Metabolism, Parkinson disease, α-synuclein, lysosomes, 616, chaperonemediated autophagy, Autophagy, alpha-Synuclein, Glucosylceramidase, Humans, ceramide, anzsrc-for: 110903 Central Nervous System, Molecular Chaperones
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