ReviewFrontiers in neuroscience2019
Prion-Like Mechanisms in Parkinson's Disease.
Review in Frontiers in neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 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
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.
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Who cites it
75 citing papers in PubMed, 1 synthesis or guideline pooled it, 133 citations in OpenAlex.
- Biofluid Detection of Pathological α-Synuclein in the Prodromal Phase of Synucleinopathies.Journal of Parkinson's disease · 2024Pooled it
- CWD prions are present in the blood of healthy-appearing, naturally infected free-ranging white-tailed deer.Scientific reports · 2026Article
- Amyloid and Tau Co-pathology in Parkinson Disease and Atypical Parkinsonism.Current neurology and neuroscience reports · 2026Review
- Dysregulation of Immune Mediators and Synaptic Plasticity in Central Nervous System Disorders.Cells · 2026Review
- Biochemical signatures of skin α-synuclein in synucleinopathies revealed by RT-QuIC assay end-product analysis.Acta neuropathologica · 2026Article
- Exploring the role of HIF-1α in pathogenesis of parkinson's disease and its potential as a therapeutic target.Molecular biology reports · 2025Review
- Physics of Protein Aggregation in Normal and Accelerated Brain Aging.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Positron emission tomography tracers for synucleinopathies.Molecular neurodegeneration · 2025Review
- Article
- Protein Misfolding in the Pathogenesis and Diagnosis of Neurodegenerative Diseases (Review).Sovremennye tekhnologii v meditsine · 2025Review
- CRISPR-Cas technologies in neurodegenerative disorders: mechanistic insights, therapeutic potential, and translational challenges.Frontiers in neurology · 2025Review
- Mass spectrometry-based proteomics for biomarker discovery in theNeuroprotection (Chichester, England) · 2024Review
- Hypoxia Pathways in Parkinson's Disease: From Pathogenesis to Therapeutic Targets.International journal of molecular sciences · 2024Review
- Single-Molecule Fingerprinting Reveals Different Growth Mechanisms in Seed Amplification Assays for Different Polymorphs of α-Synuclein Fibrils.ACS chemical neuroscience · 2024Article
- A Drosophila model for mechanistic investigation of tau protein spread.Disease models & mechanisms · 2024Article
- Review
- TGF-β1 mediates hypoxia-preconditioned olfactory mucosa mesenchymal stem cells improved neural functional recovery in Parkinson's disease models and patients.Military Medical Research · 2024Article
- An Overview of Epigenetic Changes in the Parkinson's Disease Brain.International journal of molecular sciences · 2024Review
- Disruption of Dopamine Homeostasis Associated with Alteration of Proteins in Synaptic Vesicles: A Putative Central Mechanism of Parkinson's Disease Pathogenesis.Aging and disease · 2024Review
- Inhibition of toxic metal-alpha synuclein interactions by human serum albumin.Chemical science · 2024Article
15 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Formation and aggregation of misfolded proteins in the central nervous system (CNS) is a key hallmark of several age-related neurodegenerative diseases, including Parkinson's disease (PD), Alzheimer's disease (AD), and amyotrophic lateral sclerosis (ALS). These diseases share key biophysical and biochemical characteristics with prion diseases. It is believed that PD is characterized by abnormal protein aggregation, mainly that of α-synuclein (α-syn). Of particular importance, there is growing evidence indicating that abnormal α-syn can spread to neighboring brain regions and cause aggregation of endogenous α-syn in these regions as seeds, in a "prion-like" manner. Abundant studies
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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.