ArticleMolecular neurobiology2018
Trichloroethylene and Parkinson's Disease: Risk Assessment.
Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.
- Experimental models of gut-first Parkinson's disease: A systematic review.Neurogastroenterology and motility · 2023Pooled it
- Review
- Unraveling the intersection of aging and Parkinson's disease: a collaborative roadmap for advancing research models.NPJ Parkinson's disease · 2026Review
- Developmental exposure of zebrafish to 1-Trichloromethyl-1,2,3,4-tetrahydro-beta-carboline (TaClo) elicits MPTP-like neurotoxicity.Neurotoxicology · 2025Article
- Trichloroethylene Exposure and Parkinson's Disease: Environmental Risk, Metabolic Pathways, and Mechanistic Insights.Molecular neurobiology · 2025Review
- Environmental toxins in neurodegeneration - a narrative review.Neurological research and practice · 2025Review
- Ambient Trichloroethylene Exposure and Parkinson Disease Risk in Medicare Beneficiaries.Neurology · 2025Article
- Volatile Organic Compounds (VOCs) in Neurodegenerative Diseases (NDDs): Diagnostic Potential and Analytical Approaches.Molecules (Basel, Switzerland) · 2025Review
- Targeted miRNA Delivery in Epilepsy: Mechanisms, Advances, and Therapeutic Potential.Molecular biology reports · 2025Review
- Environmental Risk Factors for Parkinson's Disease: A Critical Review and Policy Implications.Movement disorders : official journal of the Movement Disorder Society · 2025Review
- Trichloroethylene: An Update on an Environmental Contaminant with Multiple Health Effects.Annual review of pharmacology and toxicology · 2025Review
- Parkinson's Disease Progression and Exposure to Contaminated Water at Camp Lejeune.Movement disorders : official journal of the Movement Disorder Society · 2024Article
- Navigating the Neurobiology of Parkinson's: The Impact and Potential of α-Synuclein.Biomedicines · 2024Review
- LRRK2 kinase inhibition protects against Parkinson's disease-associated environmental toxicants.Neurobiology of disease · 2024Article
- Epidemiology of Parkinson's Disease: An Update.Current neurology and neuroscience reports · 2024Review
- DNA Damage and Parkinson's Disease.International journal of molecular sciences · 2024Review
- Novel Strategy to Assess the Neurotoxicity of Organic Solvents Such as Glycol Ethers: Protocol for Combining In Vitro and In Silico Methods With Human-Controlled Exposure Experiments.JMIR research protocols · 2024Article
- Evaluating Motor Dysfunction and Oxidative Stress Induced by Trichloroethylene in Wistar Rats.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Parkinson's Disease Is Predominantly an Environmental Disease.Journal of Parkinson's disease · 2024Article
- Low-dose inhalation exposure to trichloroethylene induces dopaminergic neurodegeneration in rodents.Toxicological sciences : an official journal of the Society of Toxicology · 2023Article
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 3 countries.
Funding
Abstract
This study was conducted to investigate the mechanism of action and extent of selective dopaminergic neurodegeneration caused by exposure to trichloroethylene (TCE) leading to the endogenous formation of the neurotoxin 1-trichloromethyl-1,2,3,4-tetrahydro-β-carboline (TaClo) in rodents. Beginning at 3 months of age, male C57BL/6 mice received oral TCE dissolved in vehicle for 8 months. Dopaminergic neuronal loss was assessed by nigral tyrosine hydroxylase (TH) immunoreactivity. Selective dopaminergic neurodegeneration was determined based on histological analysis of non-dopaminergic neurons in the brain. Behavioral assays were evaluated using open field activity and rotarod tests. Mitochondrial complex I activity, oxidative stress markers, and microglial activation were also examined in the substantia nigra. The level of TaClo was detected using HPLC-electrospray ionization tandem mass spectrometry. Dopaminergic neurotoxicity of TaClo was determined in midbrain organotypic cultures from rat pups. Following 8 months of TCE treatment, there was a progressive and selective loss of 50% of the dopaminergic neurons in mouse substantia nigra (SN) and about 50% loss of dopamine and 72% loss of 3,4-dihydroxyphenylacetic acid in the striatum, respectively. In addition, motor deficits, mitochondrial impairment, oxidative stress, and inflammation were measured. TaClo content was quantified in the brain after TCE treatment. In organotypic cultures, TaClo rather than TCE induced dopaminergic neuronal loss, similar to MPP
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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.