Fecal microbiota transplantation alleviated Alzheimer’s disease-like pathogenesis in APP/PS1 transgenic mice
Open accessAbstract
Alzheimer’s disease (AD) is the most common dementia in the elderly. Treatment for AD is still a difficult task in clinic. AD is associated with abnormal gut microbiota. However, little is known about the role of fecal microbiota transplantation (FMT) in AD. Here, we evaluated the efficacy of FMT for the treatment of AD. We used an APPswe/PS1dE9 transgenic (Tg) mouse model. Cognitive deficits, brain deposits of amyloid-β (Aβ) and phosphorylation of tau, synaptic plasticity as well as neuroinflammation were assessed. Gut microbiota and its metabolites short-chain fatty acids (SCFAs) were analyzed by 16S rRNA sequencing and 1 H nuclear magnetic resonance (NMR). Our results showed that FMT treatment could improve cognitive deficits and reduce the brain deposition of amyloid-β (Aβ) in APPswe/PS1dE9 transgenic (Tg) mice. These improvements were accompanied by decreased phosphorylation of tau protein and the levels of Aβ40 and Aβ42. We observed an increases in synaptic plasticity in the Tg mice, showing that postsynaptic density protein 95 (PSD-95) and synapsin I expression were increased after FMT. We also observed the decrease of COX-2 and CD11b levels in Tg mice after FMT. We also found that FMT treatment reversed the changes of gut microbiota and SCFAs. Thus, FMT may be a potential therapeutic strategy for AD.
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APP/PS1 mice exhibited significantly relieved cognitive deficits, Aβ accumulation, synaptic dysfunction, and neuroinflammation, mainly by the microglia, after FMT from healthy wild-type mice.
“Supporting this hypothesis, APP/PS1 mice exhibited significantly relieved cognitive deficits, Aβ accumulation, synaptic dysfunction, and neuroinflammation, mainly by the microglia, after FMT from healthy wild-type mice (165).”
From The Role of Short-Chain Fatty Acids From Gut Microbiota in Gut-Brain Communication (2020) · cites this paper as [165]
The Experimental design describes FMT from wild-type mice into APP/PS1 mice. The Results report improvements in cognitive tests, Aβ levels, synaptic-protein levels, and inflammatory markers after FMT. However, the Results on COX-2 and CD11b and the Discussion do not establish that microglia were the main mediator of the reduced neuroinflammation. (LLM, conf=0.86)
Experimental — accuracy not yet measuredMicrobial transplantation restores deficits in synaptic plasticity in Tg mice and decreases levels of phosphorylated tau, Aβ40 and Aβ42.
“Microbial transplantation also restores deficits in synaptic plasticity in Tg mice and decreases levels of phosphorylated tau, Aβ40 and Aβ42 [592].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [592]
Learning and memory in Tg animals can be improved through probiotic transplantation of microbiota from young control wild-type mice to Tg animals.
“Interestingly, learning and memory in Tg animals can be improved through probiotic transplantation of microbiota from young control wild-type mice to Tg animals.”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [592]
Attenuation of pathology following microbial modulation in transgenic mouse models of Alzheimer's disease supports a role for the microbiota in inflammaging in the brain.
“Attenuation of pathology following microbial modulation, in transgenic mouse models of Alzheimer’s disease [57, 115], also supports a role for the microbiota in inflammaging in the brain.”
From Fecal microbiota transfer between young and aged mice reverses hallmarks of the aging gut, eye, and brain (2022) · cites this paper as [115]
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“Supporting this hypothesis, APP/PS1 mice exhibited significantly relieved cognitive deficits, Aβ accumulation, synaptic dysfunction, and neuroinflammation, mainly by the microglia, after FMT from healthy wild-type mice (165).”
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- Authors
- Sun, J., Xu, J., Ling, Y., Wang, F., Gong, T., Yang, C., Ye, S., Ye, K., Wei, D., Song, Z., Chen, D., & Liu, J.
- Affiliations
- Wenzhou Medical University (CN)
- Corresponding author
- Liu, Jiaming
- Venue
- Translational Psychiatry
- Published
- 2019-08-05
- Volume
- 9
- Issue
- 1
- Pages
- 189-189
- ISSN
- 2158-3188 (ISSN-L)
- PMC
- PMC6683152
- OpenAlex
- W2965398438
- Cited by
- 532
- References
- 74
- Citations by year
- 2026: 60 · 2025: 91 · 2024: 92 · 2023: 81 · 2022: 85 · 2021: 83 · 2020: 36 · 2019: 3
- FWCI
- 35.37
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Translational Psychiatry (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- National Natural Science Foundation of China (81871094)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- fecal microbiota transplantation, Alzheimer's disease, APP/PS1 mice, gut microbiota, short-chain fatty acids, amyloid-beta, tau phosphorylation, synaptic plasticity, neuroinflammation, cognitive impairment, PSD-95, synapsin I, cyclooxygenase-2, CD11b
- MeSH terms
- Fecal Microbiota Transplantation, Alzheimer Disease, Animals, Disease Models, Animal, Mice, Transgenic, Neuronal Plasticity, Phosphorylation, Amyloid beta-Protein Precursor, tau Proteins, Treatment Outcome, Mice, Presenilin-1, Spatial Learning
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