Evidence map›Paper›PMID 36890624›Full record

ArticleCNS neuroscience & therapeutics2023

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

Qiwei Zhang, Wei Zhao, Yue Hou, Xinxin Song, Haiyang Yu, Jinghe Tan, Yanmeng Zhou, Han-Ting Zhang

Open access · goldAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
5.7field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 37 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Qiwei ZhangCollege of Animal Science and Veterinary Medicine, Shandong Agricultural University, Tai-an City, China.ORCID 0000-0001-8397-7471
Wei ZhaoDepartment of Pharmacology, School of Pharmacy, Qingdao University, Qingdao, China.ORCID 0000-0002-5028-1707
Yue HouInstitute of Pharmacology, Shandong First Medical University and Shandong Academy of Medical Sciences, Taian, China.
Xinxin SongInstitute of Pharmacology, Shandong First Medical University and Shandong Academy of Medical Sciences, Taian, China.
Haiyang YuInstitute of Pharmacology, Shandong First Medical University and Shandong Academy of Medical Sciences, Taian, China.
Jinghe TanCollege of Animal Science and Veterinary Medicine, Shandong Agricultural University, Tai-an City, China.
Yanmeng ZhouInstitute of Pharmacology, Shandong First Medical University and Shandong Academy of Medical Sciences, Taian, China.
Han-Ting ZhangInstitute of Pharmacology, Shandong First Medical University and Shandong Academy of Medical Sciences, Taian, China.
Shandong First Medical University · CNQingdao University · CNShandong Agricultural University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe 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.

methodThis 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.

resultsWe 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.

conclusionThe 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.

Indexed as

Alzheimer DiseaseCognitive DysfunctionGastrointestinal MicrobiomeAnimalsbeta-GlucansDisease Models, AnimalMiceMice, TransgenicNeuroinflammatory Diseasesbeta-GlucansADbrain gut axisintestinal flora metabolitesneuroinflammationβ-Glucan

Identifiers

PMID36890624
PMCPMC10173722
OpenAlexW4323652139

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.