ArticleMetallomics : integrated biometal science2014
The effects of pdr1, djr1.1 and pink1 loss in manganese-induced toxicity and the role of α-synuclein in C. elegans.
Article in Metallomics : integrated biometal science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.
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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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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
63 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.
- Rethinking 'rare'Journal of Parkinson's disease · 2025Pooled it
- The Role of Mitochondrial Quality Control in Manganese-induced Neurotoxicity.Neurotoxicity research · 2025Review
- Inhibition of Mitochondrial Complex III Causes Dopaminergic Neurodegeneration by Redox Stress inbioRxiv : the preprint server for biology · 2025Article
- The Juvenile Parkinson's Disease Mutation C212Y Impairs Mitochondrial Homeostasis in a Caenorhabditis elegans Model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Article
- The ISN Neuroscience School, Ondo 2024, Gene-environment interactions in neurological disorders: a contemporary update.Biology open · 2025Article
- Dopaminergic neurodegeneration inmicroPublication biology · 2025Article
- Dysfunctional copper homeostasis inRedox biochemistry and chemistry · 2024Article
- Copper-mediated neurotoxicity and genetic vulnerability in the background of neurodegenerative diseases in C. elegans.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- Dysfunction in atox-1 and ceruloplasmin alters labile Cu levels and consequently Cu homeostasis inFrontiers in molecular biosciences · 2024Article
- Mitochondria in the Spotlight:Cells · 2023Review
- The Role of Oxidative Stress in Manganese Neurotoxicity: A Literature Review Focused on Contributions Made by Professor Michael Aschner.Biomolecules · 2023Review
- Neurotoxicology of metals and metallic nanoparticles inAdvances in neurotoxicology · 2023Article
- The mitochondrial RNA granule modulates manganese-dependent cell toxicity.Molecular biology of the cell · 2022Article
- Review
- Manganese-Induced Toxicity inInternational journal of molecular sciences · 2022Article
- Mechanisms of manganese-induced neurotoxicity and the pursuit of neurotherapeutic strategies.Frontiers in pharmacology · 2022Review
- Ca2+ administration prevents α-synuclein proteotoxicity by stimulating calcineurin-dependent lysosomal proteolysis.PLoS genetics · 2021Article
- Effects of Manganese on Genomic Integrity in the Multicellular Model OrganismInternational journal of molecular sciences · 2021Article
- Animal Models of Autosomal Recessive Parkinsonism.Biomedicines · 2021Review
3 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
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Parkinson's disease (PD) is a neurodegenerative brain disorder characterized by selective dopaminergic (DAergic) cell loss that results in overt motor and cognitive deficits. Current treatment options exist to combat PD symptomatology, but are unable to directly target its pathogenesis due to a lack of knowledge concerning its etiology. Several genes have been linked to PD, including three genes associated with an early-onset familial form: parkin, pink1 and dj1. All three genes are implicated in regulating oxidative stress pathways. Another hallmark of PD pathophysiology is Lewy body deposition, associated with the gain-of-function genetic risk factor α-synuclein. The function of α-synuclein is poorly understood, as it shows both neurotoxic and neuroprotective activities in PD. Using the genetically tractable invertebrate Caenorhabditis elegans (C. elegans) model system, the neurotoxic or neuroprotective role of α-synuclein upon acute Mn exposure in the background of mutated pdr1, pink1 or djr1.1 was examined. The pdr1 and djr1.1 mutants showed enhanced Mn accumulation and oxidative stress that was reduced by α-synuclein. Moreover, DAergic neurodegeneration, while unchanged with Mn exposure, returned to wild-type (WT) levels for pdr1, but not djr1.1 mutants expressing α-synuclein. Taken together, this study uncovers a novel, neuroprotective role for WT human α-synuclein in attenuating Mn-induced toxicity in the background of PD-associated genes, and further supports the role of extracellular dopamine in exacerbating Mn neurotoxicity.
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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.