Cited by 40Alzheimer's disease research and treatmentsGut microbiota and healthNeuroinflammation and Neurodegeneration Mechanisms

β‐Glucan attenuates cognitive impairment of APP/PS1 mice via regulating intestinal flora and its metabolites

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Zhang, Qiwei, Zhao, Wei, Hou, Yue, Song, Xinxin, Yu, Haiyang, Tan, Jinghe, Zhou, Yanmeng, Zhang, Han‐Ting·2023·CNS Neuroscience & Therapeutics

Abstract

Background: The intestinal flora has been shown to be involved in the progression of Alzheimer's disease (AD) and can be improved by β‐glucan, a polysaccharide derived from Saccharomyces cerevisiae, which affects cognitive function through the intestinal flora. However, it is not known if this effect of β‐glucan is involved in AD. Method: This study used behavioral testing to measure cognitive function. After that, high‐throughput 16 S rRNA gene sequencing and GC–MS were used to analyze the intestinal microbiota and metabolite SCFAs of AD model mice, and further explore the relationship between intestinal flora and neuroinflammation. Finally, the expressions of inflammatory factors in the mouse brain were detected by Western blot and Elisa methods. Results: We found that appropriate supplementation of β‐glucan during the progression of AD can improve cognitive impairment and reduce A β plaque deposition. In addition, supplementation of β‐glucan can also promote changes in the composition of the intestinal flora, thereby changing the flora metabolites in the intestinal content and reduce the activation of inflammatory factors and microglia in the cerebral cortex and hippocampus through the brain‐gut axis. While reducing the expression of inflammatory factors in the hippocampus and cerebral cortex, thereby controlling neuroinflammation. Conclusion: The imbalance of the gut microbiota and metabolites plays a role in the progression of AD; β‐glucan blocks the development of AD by improving the gut microbiota and its metabolites and reducing neuroinflammation. β‐Glucan is a potential strategy for the treatment of AD by reshaping the gut microbiota and improving its metabolites.

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  • Probiotic and prebiotic interventions aimed at elevating SCFA levels have neuroprotective effects in AD mouse models by inhibiting glial activation and Aβ deposition.

    “Moreover, probiotic and prebiotic interventions aimed at elevating SCFA levels have demonstrated neuroprotective effects in AD mouse models by inhibiting glial activation and Aβ deposition.301–306”

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Authors
Zhang, Q., Zhao, W., Hou, Y., Song, X., Yu, H., Tan, J., Zhou, Y., & Zhang, H.
Affiliations
  • Shandong First Medical University (CN)
  • Qingdao University (CN)
  • College of Animal Science and Veterinary Medicine Shandong Agricultural University Tai‐an City China
Corresponding author
  • Zhou, Yanmeng
  • Zhang, Han‐Ting
Venue
CNS Neuroscience & Therapeutics
Publisher
Wiley
Published
2023-03-08
Volume
29
Issue
6
Pages
1690-1704
ISSN
  • 1755-5930 (ISSN-L)
  • 1755-5949
OpenAlex
W4323652139
Cited by
40
References
78
Citations by year
2026: 7 · 2025: 17 · 2024: 9 · 2023: 7
FWCI
7.05
Type
journal article
Language
en
Open access
Locations
  • CNS Neuroscience & Therapeutics (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
National Natural Science Foundation of China (81773717, 82073827)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
β-glucan, Alzheimer's disease, APP/PS1 mice, cognitive impairment, gut microbiota, short-chain fatty acids, gut-brain axis, neuroinflammation, microglia, amyloid plaques, hippocampus, cerebral cortex, dietary supplementation
MeSH terms
Gastrointestinal Microbiome, Neuroinflammatory Diseases, Alzheimer Disease, Animals, Disease Models, Animal, Mice, Transgenic, beta-Glucans, Mice, Cognitive Dysfunction

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