ArticleHuman molecular genetics2016
α-Synuclein interferes with the ESCRT-III complex contributing to the pathogenesis of Lewy body disease.
Article in Human molecular genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 59 citations in OpenAlex.
- Extracellular vesicles as biomarkers of disease progression and therapeutic response in patients with spinal muscular atrophy.Molecular therapy. Advances · 2026Article
- Cell-based regenerative interventions in Parkinson's disease: Overcoming pharmacological limitations.Acta pharmaceutica Sinica. B · 2026Review
- Dysregulation of the endosomal sorting complex III is linked to neurodegeneration in progressive multiple sclerosis.Brain pathology (Zurich, Switzerland) · 2026Article
- miR-132 and Its Exosomal Form in Alzheimer's Disease: Linking Epigenetic Regulation to Neurodegeneration.Molecular neurobiology · 2025Review
- Pathological α-synuclein perturbs nuclear integrity.Neurobiology of disease · 2025Article
- Review
- α-Synuclein: Multiple pathogenic roles in trafficking and proteostasis pathways in Parkinson's disease.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2024Review
- ESCRT-III: a versatile membrane remodeling machinery and its implications in cellular processes and diseases.Animal cells and systems · 2024Review
- Exosome, the glass slipper for Cinderella of cancer-bladder cancer?Journal of nanobiotechnology · 2023Review
- Novel systemic delivery of a peptide-conjugated antisense oligonucleotide to reduce α-synuclein in a mouse model of Alzheimer's disease.Neurobiology of disease · 2023Article
- The yeast guanine nucleotide exchange factor Sec7 is a bottleneck in spatial protein quality control and detoxifies neurological disease proteins.Scientific reports · 2023Article
- Acute Transcriptomic and Epigenetic Alterations at T12 After Rat T10 Spinal Cord Contusive Injury.Molecular neurobiology · 2023Article
- Disrupting the α-synuclein-ESCRT interaction with a peptide inhibitor mitigates neurodegeneration in preclinical models of Parkinson's disease.Nature communications · 2023Article
- Employing nanoparticle tracking analysis of salivary neuronal exosomes for early detection of neurodegenerative diseases.Translational neurodegeneration · 2023Review
- A Mouse Model to Test Novel Therapeutics for Parkinson's Disease: an Update on the Thy1-aSyn ("line 61") Mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- Axonal transport of Hrs is activity dependent and facilitates synaptic vesicle protein degradation.Life science alliance · 2022Article
- Alpha-Synuclein defects autophagy by impairing SNAP29-mediated autophagosome-lysosome fusion.Cell death & disease · 2021Article
- Living Proof of Activity of Extracellular Vesicles in the Central Nervous System.International journal of molecular sciences · 2021Review
- Pharmacological inhibition of nSMase2 reduces brain exosome release and α-synuclein pathology in a Parkinson's disease model.Molecular brain · 2021Article
- Extracellular Vesicles in Alzheimer's and Parkinson's Disease: Small Entities with Large Consequences.Cells · 2020Review
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
α-Synuclein (α-syn) has been implicated in neurological disorders with parkinsonism, including Parkinson's disease and Dementia with Lewy body. Recent studies have shown α-syn oligomers released from neurons can propagate from cell-to-cell in a prion-like fashion exacerbating neurodegeneration. In this study, we examined the role of the endosomal sorting complex required for transport (ESCRT) pathway on the propagation of α-syn. α-syn, which is transported via the ESCRT pathway through multivesicular bodies for degradation, can also target the degradation of the ESCRT protein-charged multivesicular body protein (CHMP2B), thus generating a roadblock of endocytosed α-syn. Disruption of the ESCRT transport system also resulted in increased exocytosis of α-syn thus potentially increasing cell-to-cell propagation of synuclein. Conversely, delivery of a lentiviral vector overexpressing CHMP2B rescued the neurodegeneration in α-syn transgenic mice. Better understanding of the mechanisms of intracellular trafficking of α-syn might be important for understanding the pathogenesis and developing new treatments for synucleinopathies.
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