Journal
AUTOPHAGY
Volume 10, Issue 7, Pages 1350-1351Publisher
LANDES BIOSCIENCE
DOI: 10.4161/auto.29074
Keywords
Parkinson disease; alpha-synuclein; glucocerebrosidase; autophagy; chaperone-mediated autophagy; lysosomes; ceramide
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Funding
- NIAAA NIH HHS [R28 AA012725, R24 AA012725] Funding Source: Medline
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Parkinson disease (PD) is a progressive neurodegenerative movement disorder characterized pathologically by abnormal SNCA/alpha-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, beta, 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.
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