ArticleMolecular neurobiology2018
Bidirectional Neural Interaction Between Central Dopaminergic and Gut Lesions in Parkinson's Disease Models.
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 58 papers, 2 of them syntheses that pooled it.
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Who cites it
58 citing papers in PubMed, 2 syntheses or guidelines pooled it, 125 citations in OpenAlex.
- Possible linking and treatment between Parkinson's disease and inflammatory bowel disease: a study of Mendelian randomization based on gut-brain axis.Journal of translational medicine · 2025Pooled it
- Gastrointestinal Dopamine in Inflammatory Bowel Diseases: A Systematic Review.International journal of molecular sciences · 2021Pooled it
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- A Novel Rat Model for Inflammatory Gut-Brain Interactions in Parkinson's Disease.The European journal of neuroscience · 2025Article
- The Absence of Gastrointestinal Redox Dyshomeostasis in the Brain-First Rat Model of Parkinson's Disease Induced by Bilateral Intrastriatal 6-Hydroxydopamine.Molecular neurobiology · 2024Article
- Exploring the nigrostriatal and digestive interplays in Parkinson's disease using dynamic total-body [European journal of nuclear medicine and molecular imaging · 2024Article
- The role of the brain renin-angiotensin system in Parkinson´s disease.Translational neurodegeneration · 2024Review
- Angiotensin type 1 receptor activation promotes neuronal and glial alpha-synuclein aggregation and transmission.NPJ Parkinson's disease · 2024Article
- Periodontal bacteria influence systemic diseases through the gut microbiota.Frontiers in cellular and infection microbiology · 2024Review
- Do Bacterial Outer Membrane Vesicles Contribute to Chronic Inflammation in Parkinson's Disease?Journal of Parkinson's disease · 2024Review
- Astrocytic insulin receptor controls circadian behavior via dopamine signaling in a sexually dimorphic manner.Nature communications · 2023Article
- α-Synuclein oligomers and fibrils: partners in crime in synucleinopathies.Neural regeneration research · 2023Article
- Gut microbiome and Parkinson's disease: Perspective on pathogenesis and treatment.Journal of advanced research · 2023Review
- Enteric glia as a player of gut-brain interactions during Parkinson's disease.Frontiers in neuroscience · 2023Review
- Advances in NURR1-Regulated Neuroinflammation Associated with Parkinson's Disease.International journal of molecular sciences · 2022Review
- Lipopolysaccharide mouse models for Parkinson's disease research: a critical appraisal.Neural regeneration research · 2022Review
- Defining the unknowns for cell therapies in Parkinson's disease.Disease models & mechanisms · 2022Article
- Neuroinflammation and Parkinson's Disease-From Neurodegeneration to Therapeutic Opportunities.Cells · 2022Review
- Gut microenvironmental changes as a potential trigger in Parkinson's disease through the gut-brain axis.Journal of biomedical science · 2022Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The exact mechanism of gut dysfunction in Parkinson's disease and, conversely, the role of gut pathology in brain dopaminergic degeneration are controversial. We investigated the effects of nigral lesions on the colonic neurotransmission, the effect of gut inflammation on the nigrostriatal dopaminergic function, and the possible involvement of the vagus nerve and the local renin-angiotensin system (RAS). Nigrostriatal dopamine depletion was performed by bilateral injection 6-hydroxydopamine, and gut inflammation was induced by dextran sulfate sodium salt treatment in rats and mice, respectively, with or without vagal disruption. A decrease in central dopamine levels induced a decrease in colonic dopamine types 1 and 2 receptor expression together with an increase in the colonic levels of dopamine and a decrease in the levels of acetylcholine, which may explain a decrease in gut motility. Central dopaminergic depletion also induced an increase in the colonic levels of inflammatory and oxidative stress markers together with activation of the pro-inflammatory arm of the local RAS. Mice with acute (1 week) or subchronic (3 weeks) gut inflammation did not show a significant increase in colonic α-synuclein and phosphorylated α-synuclein expression during this relatively short survival period. Interestingly, we observed early changes in the nigrostriatal dopaminergic homeostasis, dopaminergic neuron death, and increased levels of nigral pro-inflammatory markers and RAS pro-inflammatory activity. The present results show that a dysregulation of the neural bidirectional gut-brain interaction may explain the early gut disturbances observed in parkinsonian patients, and also the increase in vulnerability of nigral dopaminergic neurons after gut inflammation.
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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.