Trimethylamine N-Oxide Exacerbates Neuroinflammation and Motor Dysfunction in an Acute MPTP Mice Model of Parkinson’s Disease
Open accessAbstract
Observational studies have shown abnormal changes in trimethylamine N-oxide (TMAO) levels in the peripheral circulatory system of Parkinson’s disease (PD) patients. TMAO is a gut microbiota metabolite that can cross the blood–brain barrier and is strongly related to neuroinflammation. Neuroinflammation is one of the pathological drivers of PD. Herein, we investigated the effect of TMAO on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD model mice. TMAO pretreatment was given by adding 1.5% (w/v) TMAO to the drinking water of the mice for 21 days; then, the mice were administered MPTP (20 mg/kg, i.p.) four times a day to construct an acute PD model. Their serum TMAO concentrations, motor function, dopaminergic network integrity, and neuroinflammation were then assayed. The results showed that TMAO partly aggravated the motor dysfunction of the PD mice. Although TMAO had no effect on the dopaminergic neurons, TH protein content, and striatal DA level in the PD mice, it significantly reduced the striatal 5-HT levels and aggravated the metabolism of DA and 5-HT. Meanwhile, TMAO significantly activated glial cells in the striatum and the hippocampi of the PD mice and promoted the release of inflammatory cytokines in the hippocampus. In summary, higher-circulating TMAO had adverse effects on the motor capacity, striatum neurotransmitters, and striatal and hippocampal neuroinflammation in PD mice.
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TMAO levels are elevated in plasma and cerebrospinal fluid of individuals with mild cognitive impairment and Alzheimer's disease, and TMAO can traverse the blood-brain barrier and contribute to neurodegeneration by inducing microglial and astrocytic activation.
“Importantly, elevated levels of TMAO have been observed in the plasma and cerebrospinal fluid (CSF) of individuals with MCI and AD.409,410 Several studies have shown that TMAO has the ability to traverse the BBB and contribute to neurodegeneration by inducing microglial and astrocytic activation.411–414”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [413]
TMAO is associated with neuroinflammation by inducing microglial and astrocytic activation.
“TMAO is also associated with neuroinflammation by inducing microglial and astrocytic activation.”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [413]
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- Authors
- Quan, W., Qiao, C.-M., Niu, G.-Y., Wu, J., Zhao, L.-P., Cui, C., Zhao, W.-J., & Shen, Y.-Q.
- Affiliations
- Jiangnan University (CN)
- Department of Neurodegeneration and Injury, Wuxi School of Medicine, Jiangnan University, Wuxi 214122, China
- Corresponding author
- Shen, Yan-Qin
- Venue
- Brain Sciences
- Publisher
- MDPI AG
- Published
- 2023-05-12
- Volume
- 13
- Issue
- 5
- Pages
- 790
- ISSN
- 2076-3425 (ISSN-L)
- PMC
- PMC10216692
- OpenAlex
- W4376278723
- Cited by
- 49
- References
- 40
- Citations by year
- 2026: 17 · 2025: 19 · 2024: 13
- FWCI
- 8.29
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Brain Sciences (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- The National Natural Science Foundation of China (82171429, 81771384, KYCX22_2436)
- Postgraduate Research & Practice Innovation Program of Jiangsu Province (82171429, 81771384, KYCX22_2436)
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Keywords
- trimethylamine N-oxide, Parkinson's disease, MPTP-induced neurotoxicity, neuroinflammation, motor impairment, gut microbiota metabolites, blood-brain barrier, dopaminergic neurons, serotonin metabolism, striatum, hippocampus, glial activation, inflammatory cytokines, gut-brain axis
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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