Trimethylamine N-oxide aggravated cognitive impairment from APP/PS1 mice and protective roles of voluntary exercise
Abstract
To determine whether trimethylamine N-oxide (TMAO) would aggravate cognitive dysfunction from APP/PS1 mice and the potential protective effects of voluntary wheel running (VWR). TMAO impaired learning and memory abilities, and exercise reversed TMAO induced cognitive impairment. Serum TMAO, choline, betaine and TMA were significantly elevated from TMAO group, while exercise group had decreased TMAO, betaine and TMA level. TMAO group has significantly upregulated BACE1 from both hippocampus and cortex, also increased cathepsin B, p-Tau at Ser396&Ser404, GFAP, p-NF-κB p65 in cortex, while reduced BDNF, synaptophysin and PSD95 in hippocampus, also reduced occludin and ZO-1 from cortex, and reduced occludin from colon. In contrast, BACE1 from both hippocampus and cortex, also cathepsin B and p-Tauser396 from cortex were reduced, BDNF, snaptophysin, and PSD95 from hippocampus, ZO-1 from cortex, and occludin from colon were elevated post exercise compared to TMAO group. Exercise elevated α diversity index of cecal content, and TMAO and exercise affected gut microbiota profiles differentially. In conclusion, TMAO led to gut microbiota dysbiosis, impaired gut-brain integrity, elevated neuroinflammation, Aβ pathology and tau phosphorylation, disordered synaptic function; and exercise could reverse TMAO induced cognitive dysfunction via improving the above markers. The potential deleterious effects of TMAO on cognitive function need to be validated in humans, also dosages of exercise for exerting neuroprotective effects against TMAO induced cognitive impairment.
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TMAO supplementation induces cognitive impairment in APP/PS1 mice by promoting neuroinflammation, amyloid-beta and tau pathology, and disrupting intestinal barrier and blood-brain barrier integrity.
“TMAO supplementation has been shown to induce cognitive impairment in APP/PS1 mice by promoting neuroinflammation, Aβ and tau pathology (Fig. 3b). Interestingly, the study also found that TMAO supplementation disrupted the integrity of the intestinal barrier and BBB.414”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [414]
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 [414]
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 [414]
APP/PS1 mice fed with a TMAO-supplemented diet manifested reduced occludin and ZO-1 expression in the parietal cortex, along with increased microglial and astrocytic activation.
“APP/PS1 mice fed with a TMAO-supplemented diet manifested reduced occludin and ZO-1 expression in the parietal cortex, along with increased microglial and astrocytic activation.”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [414]
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- Authors
- Zhang, Y., Wang, G., Li, R., Liu, R., Yu, Z., Zhang, Z., & Wan, Z.
- Affiliations
- Soochow University (CN)
- Zhengzhou University (CN)
- Corresponding author
- Zhang, Ying
- Zhang, Zengli
- Wan, Zhongxiao
- Venue
- Neurochemistry International
- Publisher
- Elsevier BV
- Published
- 2023-01
- Volume
- 162
- Pages
- 105459
- ISSN
- 0197-0186 (ISSN-L)
- OpenAlex
- W4310291828
- Cited by
- 37
- References
- 40
- Citations by year
- 2026: 14 · 2025: 14 · 2024: 8 · 2023: 1
- FWCI
- 3.56
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- Neurochemistry International (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Key University Science Research Project of Jiangsu Province (21KJB310021)
- National Natural Science Foundation of China (81872609)
- Priority Academic Program Development of Jiangsu Higher Education Institutions
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- trimethylamine N-oxide, cognitive impairment, APP/PS1 mice, Alzheimer's disease, voluntary wheel running, gut dysbiosis, gut-brain axis, neuroinflammation, tau phosphorylation, amyloid-beta pathology, BACE1, synaptic function, tight junctions
- MeSH terms
- Animals, Betaine, Cathepsin B, Choline, Methylamines, Motor Activity, Exercise, Aspartic Acid Endopeptidases, Brain-Derived Neurotrophic Factor, Mice, Amyloid Precursor Protein Secretases, Cognitive Dysfunction, Occludin
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