ReviewMovement disorders : official journal of the Movement Disorder Society2016
Lysosomal trafficking defects link Parkinson's disease with Gaucher's disease.
Review in Movement disorders : official journal of the Movement Disorder Society, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 2 of them syntheses that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
39 citing papers in PubMed, 2 syntheses or guidelines pooled it, 57 citations in OpenAlex.
- Meta-analysis of the association of prosaposin polymorphisms rs4747203 and rs885828 with risk of Parkinson's disease.Acta neurologica Belgica · 2024Pooled it
- Role of Lysosomal Gene Variants in Modulating GBA-Associated Parkinson's Disease Risk.Movement disorders : official journal of the Movement Disorder Society · 2022Pooled it
- A sensitive LC‑MS/MS method for the simultaneous quantification of hexosylceramides and hexosylsphingosines, their precursors and metabolites in cells, plasma, and tissue homogenates.Analytical and bioanalytical chemistry · 2026Article
- Two lysosomal genes ATP13A2 and GBA1 interact to drive neurodegeneration.Molecular neurodegeneration · 2026Article
- The Role of Cardiolipin in Brain Bioenergetics, Neuroinflammation, and Neurodegeneration.Molecular neurobiology · 2025Review
- Lack of significant ganglioside changes inBiochemistry and biophysics reports · 2025Article
- Relationship of cognitive decline with glucocerebrosidase activity and amyloid-beta 42 in DLB and PD.Annals of clinical and translational neurology · 2025Article
- The C. elegans gba-3 gene encodes a glucocerebrosidase that exacerbates α-synuclein-mediated impairments in deletion mutants.Translational neurodegeneration · 2025Article
- Review
- Axonal Transport of Lysosomes Is Unaffected in Glucocerebrosidase-Inhibited iPSC-Derived Forebrain Neurons.eNeuro · 2023Article
- Recombinant pro-CTSD (cathepsin D) enhances SNCA/α-Synuclein degradation in α-Synucleinopathy models.Autophagy · 2022Article
- Regulation of neuronal autophagy and the implications in neurodegenerative diseases.Neurobiology of disease · 2022Review
- MANF InhibitsOxidative medicine and cellular longevity · 2022Article
- Disease-, region- and cell type specific diversity of α-synuclein carboxy terminal truncations in synucleinopathies.Acta neuropathologica communications · 2021Article
- Profiling the Biochemical Signature of GBA-Related Parkinson's Disease in Peripheral Blood Mononuclear Cells.Movement disorders : official journal of the Movement Disorder Society · 2021Article
- Vesicle trafficking and lipid metabolism in synucleinopathy.Acta neuropathologica · 2021Review
- Sphingolipids as Regulators of Neuro-Inflammation and NADPH Oxidase 2.Neuromolecular medicine · 2021Review
- Interaction between Parkin andCells · 2021Review
- Simple and Complex Sugars in Parkinson's Disease: a Bittersweet Taste.Molecular neurobiology · 2020Review
- Organoid and pluripotent stem cells in Parkinson's disease modeling: an expert view on their value to drug discovery.Expert opinion on drug discovery · 2020Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Lysosomal dysfunction has been implicated in multiple diseases, including lysosomal storage disorders such as Gaucher's disease, in which loss-of-function mutations in the GBA1 gene encoding the lysosomal hydrolase β-glucocerebrosidase result in lipid substrate accumulation. In Parkinson's disease, α-synuclein accumulates in Lewy bodies and neurites contributing to neuronal death. Previous clinical and genetic evidence has demonstrated an important link between Parkinson's and Gaucher's disease, as GBA1 mutations and variants increase the risk of Parkinson's and Parkinson's patients exhibit decreased β-glucocerebrosidase activity. Using human midbrain neuron cultures, we have found that loss of β-glucocerebrosidase activity promotes α-synuclein accumulation and toxicity, whereas α-synuclein accumulation further contributes to decreased lysosomal β-glucocerebrosidase activity by disrupting β-glucocerebrosidase trafficking to lysosomes. Moreover, α-synuclein accumulation disrupts trafficking of additional lysosomal hydrolases, further contributing to lysosomal dysfunction and neuronal dyshomeostasis. Importantly, promoting β-glucocerebrosidase activity reduces α-synuclein accumulation and rescues lysosomal and neuronal dysfunction, suggesting that β-glucocerebrosidase may be an important therapeutic target for advancing drug discovery in synucleinopathies including Parkinson's disease. © 2016 International Parkinson and Movement Disorder Society.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.