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Akkermansia muciniphila reduces neuroinflammation and Aβ deposition via tryptophan metabolism in the APP/PS1 mouse model of Alzheimer’s disease
Akkermansia muciniphila may reduce brain inflammation and amyloid buildup through tryptophan metabolism in a mouse model of Alzheimer's disease
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Abstract
A. muciniphila administration improves cognitive deficits and reduces amyloid-beta (Aβ) deposition in APP/PS1 mice.
- A. muciniphila administration significantly alters gut microbiota diversity and composition.
- The treatment increases the production of 62 metabolites, including such as butyric acid and acetic acid.
- A. muciniphila administration is associated with decreased levels of 28 metabolites, including isoleucine and N-acetylneuraminic acid.
- Cytokine analysis shows reduced levels of pro-inflammatory cytokines and increased levels of anti-inflammatory cytokines following A. muciniphila administration.
- A positive correlation exists between the increased levels of certain metabolites and cognitive function indicators.
- Cognitive deficits, neuroinflammation, and Aβ deposition are alleviated through the AhR/NF-κB/NLRP3 signaling pathway in APP/PS1 mice.
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Key numbers
2×
Increase in cognitive performance
Performance improvement in Morris Water Maze test for A. muciniphila-treated mice vs. untreated mice.
28% decrease
Reduction in Aβ plaque deposition
Reduction of Aβ plaques in the hippocampus and cortex of A. muciniphila-treated APP/PS1 mice.