ArticleNPJ Parkinson's disease2024
Cell-to-cell transmitted alpha-synuclein recapitulates experimental Parkinson's disease.
Article in NPJ Parkinson's disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
What it found
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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.
The trial behind it
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- A bibliometric analysis of alpha-synuclein in Parkinson's disease from 2015 to 2024.Frontiers in neurologyPooled it
- Rebalancing α-Synuclein Clearance: Novel Therapeutic Frontiers in Parkinson's Disease.Neuromolecular medicine · 2026Review
- Are Signal Peptides Hidden Regulators of Neurodegenerative Disease?Biomedicines · 2026Review
- Mitochondrial Dysfunction: From Molecular Mechanisms to Modern Approaches for Basic and Clinical Research.Biomedicines · 2026Review
- Distinct Molecular Mechanisms Underlie Modulation of Seeded α-Synuclein Aggregation and Toxicity by Salvianolic Acid B and Dihydromyricetin.International journal of molecular sciences · 2026Article
- Propagation of α-synuclein pathology: models, mechanisms and future goals.Molecular neurodegeneration advances · 2026Review
- From dysbiosis to dysfunction: specific gut microbes and metabolites in the pathogenesis of Parkinson's disease.Sustainable microbiology · 2026Review
- Hidden faces of alpha-synuclein: Cryo-EM revelation of fibril polymorphs driven by disease, mutations, and PTMs.BBA advances · 2026Review
- Elevated hexosylceramides in Parkinson's disease cause gene upregulations in neurons mimicking responses to pathogens.NPJ Parkinson's disease · 2025Article
- Optogenetics to biomolecular phase separation in neurodegenerative diseases.Molecules and cells · 2025Review
- Effect of hydrogen sulfide on alpha-synuclein aggregation and cell viability.Scientific reports · 2025Article
- Overview of Metformin and Neurodegeneration: A Comprehensive Review.Pharmaceuticals (Basel, Switzerland) · 2025Review
- A comprehensive review of natural compounds and their structure-activity relationship in Parkinson's disease: exploring potential mechanisms.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Astrocytes-associated research in Parkinson's disease: an explored trends analysis.Frontiers in aging neuroscience · 2025Article
- Novel Glitazones Protect Rotenone-induced Parkinsonism in Mouse Models by Targeting PGC1α.Current drug targets · 2025Article
- Manganese Exposure Enhances the Release of Misfolded α-Synuclein via Exosomes by Impairing Endosomal Trafficking and Protein Degradation Mechanisms.International journal of molecular sciences · 2024Article
- Targets to Search for New Pharmacological Treatment in Idiopathic Parkinson's Disease According to the Single-Neuron Degeneration Model.Biomolecules · 2024Review
- Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 4 countries.
Funding
Abstract
Parkinson's disease is characterized by a progressive accumulation of alpha-Synuclein (αSyn) neuronal inclusions called Lewy bodies in the nervous system. Lewy bodies can arise from the cell-to-cell propagation of αSyn, which can occur via sequential steps of secretion and uptake. Here, by fusing a removable short signal peptide to the N-terminus of αSyn, we developed a novel mouse model with enhanced αSyn secretion and cell-to-cell transmission. Expression of the secreted αSyn in the mouse brain was under the control of a novel hybrid promoter in combination with adeno-associated virus serotype 9 (AAV9). This combination of promoter and viral vector induced a robust expression in neurons but not in the glia of injected mice. Biochemical characterization of the secreted αSyn revealed that, in cultured cells, this protein is released to the extracellular milieu via conventional secretion. The released αSyn is then internalized and processed by acceptor cells via the endosome-lysosome pathway indicating that the secreted αSyn is cell-to-cell transmitted. The secreted αSyn is aggregation-prone and amyloidogenic, and when expressed in the brain of wild-type non-transgenic mice, it induces a Parkinson's disease-like phenotype that includes a robust αSyn pathology in the substantia nigra, neuronal loss, neuroinflammation, and motor deficits, all the key features of experimental animal models of Parkinson's disease. In summary, a novel animal model of Parkinson's disease based on enhanced cell-to-cell transmission of αSyn was developed. The neuron-produced cell-to-cell transmitted αSyn triggers all phenotypic features of experimental Parkinson's disease in mice.
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What OpenQuestion holds
Registered trials
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.