ArticleJournal of neuropathology and experimental neurology2017
Oral Exposure to Paraquat Triggers Earlier Expression of Phosphorylated α-Synuclein in the Enteric Nervous System of A53T Mutant Human α-Synuclein Transgenic Mice.
Article in Journal of neuropathology and experimental neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 2 of them syntheses that pooled it.
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Who cites it
24 citing papers in PubMed, 2 syntheses or guidelines pooled it, 46 citations in OpenAlex.
- Enteric Nervous System Damage by Food Contaminants: A Pathway to Neurodegeneration?Comprehensive reviews in food science and food safety · 2026Pooled it
- Experimental models of gut-first Parkinson's disease: A systematic review.Neurogastroenterology and motility · 2023Pooled it
- The microbiota at the interface of environmental toxicants and the brain.Cell metabolism · 2026Review
- Chronic Paraquat Neurotoxicity and Dopaminergic Degeneration: A Mechanistic Review.Chemistry & biodiversity · 2026Review
- Environmental toxins in neurodegeneration - a narrative review.Neurological research and practice · 2025Review
- Environmental Risk Factors for Parkinson's Disease: A Critical Review and Policy Implications.Movement disorders : official journal of the Movement Disorder Society · 2025Review
- Agricultural paraquat dichloride use and Parkinson's disease in California's Central Valley.International journal of epidemiology · 2024Article
- New Pieces for an Old Puzzle: Approaching Parkinson's Disease from Translatable Animal Models, Gut Microbiota Modulation, and Lipidomics.Nutrients · 2023Review
- Pesticides and the Microbiome-Gut-Brain Axis: Convergent Pathways in the Pathogenesis of Parkinson's Disease.Journal of Parkinson's disease · 2023Review
- Gut microenvironmental changes as a potential trigger in Parkinson's disease through the gut-brain axis.Journal of biomedical science · 2022Review
- Environmental triggers of Parkinson's disease - Implications of the Braak and dual-hit hypotheses.Neurobiology of disease · 2022Review
- Gut-brain axis: Review on the association between Parkinson's disease and plant lectins.Archive of clinical cases · 2022Review
- Chronic Exposure to Paraquat Induces Alpha-Synuclein Pathogenic Modifications inInternational journal of molecular sciences · 2021Article
- Neurotoxin-Induced Rodent Models of Parkinson's Disease: Benefits and Drawbacks.Neurotoxicity research · 2021Review
- Immunomorphological Changes in Neuronal and Non-Neuronal Structures in the Rat Intestine in a Toxin-Induced Model of Parkinsonism.Bulletin of experimental biology and medicine · 2021Article
- Molecular Communication Between Neuronal Networks and Intestinal Epithelial Cells in Gut Inflammation and Parkinson's Disease.Frontiers in medicine · 2021Review
- Parkinson disease and the gut: new insights into pathogenesis and clinical relevance.Nature reviews. Gastroenterology & hepatology · 2020Review
- Heterogeneity of dopamine release sites in health and degeneration.Neurobiology of disease · 2020Review
- Parkinson's Disease and the Gut: Future Perspectives for Early Diagnosis.Frontiers in neuroscience · 2020Review
- Selective vulnerability in α-synucleinopathies.Acta neuropathologica · 2019Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The misfolded α-synuclein protein, phosphorylated at serine 129 (pSer129 α-syn), is the hallmark of Parkinson disease (PD). Detected also in the enteric nervous system (ENS), it supports the recent theory that PD could start in the gut, rather than the brain. In a previous study, using a transgenic mouse model of human synucleinopathies expressing the A53T mutant α-synuclein (TgM83), in which a neurodegenerative process associated with α-synuclein occurs spontaneously in the brain, we have shown earlier onset of pSer129 α-syn in the ENS. Here, we used this model to study the impact of paraquat (PQ) a neurotoxic herbicide incriminated in PD in agricultural workers) on the enteric pSer129 α-syn expression in young mice. Orally delivered in the drinking water at 10 mg/kg/day for 6-8 weeks, the impact of PQ was measured in a time-dependent manner on weight, locomotor abilities, pSer129 α-syn, and glial fibrillary acidic protein (GFAP) expression levels in the ENS. Remarkably, pSer129 α-syn was detected in ENS earlier under PQ oral exposure and enteric GFAP expression was also increased. These findings bring additional support to the theory that neurotoxic agents such as PQ initiate idiopathic PD after oral delivery.
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Registered trials
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