ReviewTranslational neurodegeneration2017
Mini-review on initiatives to interfere with the propagation and clearance of alpha-synuclein in Parkinson's disease.
Review in Translational neurodegeneration, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- OTUD5 Protects Dopaminergic Neurons by Promoting the Degradation of α-Synuclein in Parkinson's Disease Model.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Cofilin 1 promotes the pathogenicity and transmission of pathological α-synuclein in mouse models of Parkinson's disease.NPJ Parkinson's disease · 2022Article
- Parkinson's disease and the gastrointestinal microbiome.Journal of neurology · 2020Review
- Case of Early-Onset Parkinson's Disease in a Heterozygous Mutation Carrier of theJournal of personalized medicine · 2019Article
- Leveraging the interplay of nanotechnology and neuroscience: Designing new avenues for treating central nervous system disorders.Advanced drug delivery reviews · 2019Review
- Prion-Like Mechanisms in Parkinson's Disease.Frontiers in neuroscience · 2019Review
- Multi-Pronged Interactions Underlie Inhibition of α-Synuclein Aggregation by β-Synuclein.Journal of molecular biology · 2018Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this mini-review, we summarize recent findings relating to the prion-like propagation of α-synuclein (α-syn) and the development of novel therapeutic strategies to target synucleinopathy in Parkinson's disease (PD). We link the Braak's staging hypothesis of PD with the recent evidence from in-vivo and in-vitro studies for the prion-like cell-to-cell propagation of α-syn (via exocytosis and endocytosis). The classical accumulation of aggregated α-syn in PD may result from an increased production or a failure in the mechanisms of clearance of α-syn. We discuss novel agents, currently in clinical trial for PD including the ones that impact the aggregation of α-syn and others that interfere with α-syn endocytosis as a means to target the progression of the disease.
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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.