ReviewCurrent opinion in neurology2016
How strong is the evidence that Parkinson's disease is a prion disorder?
Review in Current opinion in neurology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 72 citations in OpenAlex.
- Simvastatin as a Potential Disease-Modifying Therapy for Patients with Parkinson's Disease: Rationale for Clinical Trial, and Current Progress.Journal of Parkinson's disease · 2017Trial
- Exposure to fibrillar proteins leads to widespread infiltration but only mild tau pathology in cortical organoids.iScience · 2026Article
- A Neuronal Cell Line Model for Studying Camel Prions.Pathogens (Basel, Switzerland) · 2026Article
- Review
- Contrasting roles of autophagy in cellular prion infection.Autophagy · 2025Article
- Single-domain antibody-based protein degrader for synucleinopathies.Molecular neurodegeneration · 2024Article
- Single-Domain Antibody-Based Protein Degrader for Synucleinopathies.bioRxiv : the preprint server for biology · 2024Article
- Dysbiosis of the gut microbiota and its effect on α-synuclein and prion protein misfolding: consequences for neurodegeneration.Frontiers in cellular and infection microbiology · 2024Review
- Role of exosomes in the pathogenesis of inflammation in Parkinson's disease.Neural regeneration research · 2022Review
- Binding Stability of Antibody-α-Synuclein Complexes Predicts the Protective Efficacy of Anti-α-synuclein Antibodies.Molecular neurobiology · 2022Article
- Article
- Protection of dopaminergic neurons in hemiparkinsonian monkeys by flavouring ingredient glyceryl tribenzoate.NeuroImmune pharmacology and therapeutics · 2022Article
- Efficacy and immunogenicity of MultiTEP-based DNA vaccines targeting human α-synuclein: prelude for IND enabling studies.NPJ vaccines · 2022Article
- Extracellular Vesicles for the Diagnosis and Treatment of Parkinson's Disease.Aging and disease · 2021Review
- Mechanisms of Neurodegeneration in Various Forms of Parkinsonism-Similarities and Differences.Cells · 2021Review
- Gene Therapy to Modulate Alpha-Synuclein in Synucleinopathies.Journal of Parkinson's disease · 2021Review
- Effects of Alpha-Synuclein Targeted Antisense Oligonucleotides on Lewy Body-Like Pathology and Behavioral Disturbances Induced by Injections of Pre-Formed Fibrils in the Mouse Motor Cortex.Journal of Parkinson's disease · 2021Article
- Contributions of Molecular and Optical Techniques to the Clinical Diagnosis of Alzheimer's Disease.Brain sciences · 2020Review
- Neurocognitive and psychiatric disorders-related axonal degeneration in Parkinson's disease.Journal of neuroscience research · 2020Article
- Neurodegenerative Diseases - Is Metabolic Deficiency the Root Cause?Frontiers in neuroscience · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
purpose of reviewWe describe evidence supporting the hypothesis that α-synuclein has a prion-like role in Parkinson's disease and related α-synucleinopathies, and discuss how this novel thinking impacts the development of diagnostics and disease-modifying therapies. RECENT
findingsObservations that immature dopamine neurons grafted to Parkinson's disease patients can develop Lewy bodies triggered a surge of interest in the putative prion-like properties of α-synuclein. We recount results from experiments which confirm that misfolded α-synuclein can exhibit disease-propagating properties, and describe how they relate to the spreading of α-synuclein aggregates in α-synucleinopathies. We share insights into the underlying molecular mechanisms and their relevance to novel therapeutic targets. Finally, we discuss what the initial triggers of α-synuclein misfolding might be, where in the body the misfolding events might take place, and how this can instruct development of novel diagnostic tools. We speculate that differences in anatomical trigger sites and variability in α-synuclein fibril structure can contribute to clinical differences between α-synucleinopathies. SUMMARY: The realization that α-synuclein pathology can propagate between brain regions in neurodegenerative diseases has deepened and expanded our understanding of potential pathogenic processes which can lead to the development of novel diagnostic tools as well as the identification of new therapeutic targets.
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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.