ReviewJournal of Parkinson's disease2018
Modeling Parkinson's Disease in C. elegans.
Review in Journal of Parkinson's disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 102 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
102 citing papers in PubMed, 213 citations in OpenAlex.
- Pyran compound 7r exerts neuroprotective effects against Parkinson's disease via modulating oxidative stress and autophagy.iScience · 2026Article
- Dimethyl fumarate ameliorates quinolinic acid-induced ageing and neurodegeneration in Caenorhabditis elegans.Biogerontology · 2026Article
- Article
- Marine bacterium Stutzerimonas stutzeri mitigates Parkinson's disease pathology in C. elegans via ferroptosis modulation.Scientific reports · 2026Article
- In Vivo Screen of Parkinson's Disease GWAS Risk Genes IdentifiesThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Unraveling the core: hub genes bridging familial and sporadic Parkinson's disease.Journal of neurology · 2026Article
- Article
- Review
- A commercially available DJ-1 antibody does not detectmicroPublication biology · 2026Article
- Propagation of α-synuclein pathology: models, mechanisms and future goals.Molecular neurodegeneration advances · 2026Review
- Mutations in the Key Autophagy Tethering Factor EPG5 Link Neurodevelopmental and Neurodegenerative Disorders Including Early-Onset Parkinsonism.Annals of neurology · 2025Article
- Pantoea piersonii IIIF1SW-P2Scientific reports · 2025Article
- The dopaminergic system ofRoyal Society open science · 2025Review
- Review
- Hyperoside extends lifespan in Caenorhabditis elegans through SEK-1/PMK-1/SKN-1 pathway.Biogerontology · 2025Article
- Conserved lipid metabolic reprogramming confers hypoxic and aging resilience.bioRxiv : the preprint server for biology · 2025Article
- Article
- Integrated Behavioral and Proteomic Characterization of MPPInternational journal of molecular sciences · 2025Article
- Article
- Neurogrit Gold Attenuates 6-OHDA-Induced Dopaminergic Neurodegeneration in Parkinson's Model of Caenorhabditis elegans by Reducing α-Synuclein Accumulation and Pink/Pdr-1 Driven Mitochondrial Dysfunction.CNS neuroscience & therapeutics · 2025Article
42 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Parkinson's disease (PD) is an adult onset neurodegenerative disease that is characterized by selective degeneration of neurons primarily in the substantia nigra. At present, the pathogenesis of PD is incompletely understood and there are no neuroprotective treatments available. Accurate animal models of PD provide the opportunity to elucidate disease mechanisms and identify therapeutic targets. This review focuses on C. elegans models of PD, including both genetic and toxicant models. This microscopic worm offers several advantages for the study of PD including ease of genetic manipulation, ability to complete experiments rapidly, low cost, and ability to perform large scale screens for disease modifiers. A number of C. elegans models of PD have been generated including transgenic worms that express α-synuclein or LRRK2, and worms with deletions in PRKN/pdr-1, PINK1/pink-1, DJ-1/djr-1.1/djr-1.2 and ATP13A2/catp-6. These worms have been shown to exhibit multiple phenotypic deficits including the loss of dopamine neurons, disruption of dopamine-dependent behaviors, increased sensitivity to stress, age-dependent aggregation, and deficits in movement. As a result, these phenotypes can be used as outcome measures to gain insight into disease pathogenesis and to identify disease modifiers. In this way, C. elegans can be used as an experimental tool to elucidate mechanisms involved in PD and to find novel therapeutic targets that can subsequently be validated in other models.
Indexed as
Identifiers
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.