Evidence map›Paper›PMID 41715194›Full record

ArticleAlzheimer's research & therapy2026

Akkermansia muciniphila reduces neuroinflammation and Aβ deposition via tryptophan metabolism in the APP/PS1 mouse model of Alzheimer's disease.

Binghua Wang, Miaomiao Pan, Liu Yang, Jietian Xu, Chang Ye, Yunhan Li, Qianyi Gong, Changqian Liu, Lanfang Li, Jie Qin and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Alzheimer's research & therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Neuroprotective effects ofFrontiers in nutrition · 2026
    Article
  7. Article
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

13 authors.

Binghua Wang *Department of Human Anatomy, Histology & Embryology, School of Basic Medical Sciences; Department of Central Laboratory, Clinical Laboratory, Jing'an District Central Hospital, Fudan University, Shanghai, 200032, China.
Miaomiao Pan *MOE/NHC/CAMS Key Lab of Medical Molecular Virology, School of Basic Medical Sciences, & National Clinical Research Center for Aging and Medicine, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
Liu Yang *College of Food Science and Engineering, Jilin Agricultural University, Changchun, 130118, China.
Jietian XuDepartment of Human Anatomy, Histology & Embryology, School of Basic Medical Sciences; Department of Central Laboratory, Clinical Laboratory, Jing'an District Central Hospital, Fudan University, Shanghai, 200032, China.
Chang YeDepartment of Human Anatomy, Histology & Embryology, School of Basic Medical Sciences; Department of Central Laboratory, Clinical Laboratory, Jing'an District Central Hospital, Fudan University, Shanghai, 200032, China.
Yunhan LiDepartment of Human Anatomy, Histology & Embryology, School of Basic Medical Sciences; Department of Central Laboratory, Clinical Laboratory, Jing'an District Central Hospital, Fudan University, Shanghai, 200032, China.
Qianyi GongDepartment of Human Anatomy, Histology & Embryology, School of Basic Medical Sciences; Department of Central Laboratory, Clinical Laboratory, Jing'an District Central Hospital, Fudan University, Shanghai, 200032, China.
Changqian LiuDepartment of Human Anatomy, Histology & Embryology, School of Basic Medical Sciences; Department of Central Laboratory, Clinical Laboratory, Jing'an District Central Hospital, Fudan University, Shanghai, 200032, China.
Lanfang LiDepartment of Human Anatomy, Histology & Embryology, School of Basic Medical Sciences; Department of Central Laboratory, Clinical Laboratory, Jing'an District Central Hospital, Fudan University, Shanghai, 200032, China.
Jie QinDepartment of Human Anatomy, Histology & Embryology, School of Basic Medical Sciences; Department of Central Laboratory, Clinical Laboratory, Jing'an District Central Hospital, Fudan University, Shanghai, 200032, China.
Dayong RenCollege of Food Science and Engineering, Jilin Agricultural University, Changchun, 130118, China. rendayong@jlau.edu.cn.
Chao ZhaoMOE/NHC/CAMS Key Lab of Medical Molecular Virology, School of Basic Medical Sciences, & National Clinical Research Center for Aging and Medicine, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, 200032, China. czhao@fudan.edu.cn.
Chunmin LiangDepartment of Human Anatomy, Histology & Embryology, School of Basic Medical Sciences; Department of Central Laboratory, Clinical Laboratory, Jing'an District Central Hospital, Fudan University, Shanghai, 200032, China. cmliang@fudan.edu.cn.

Funding

National Natural Science Foundation of China U24A2072Shanghai Clinical Research Foundation of China 20224Y0251Training Plan for Outstanding Young Talents in Medical and Health Care of Jing'an District of Shanghai 2024YQ01
6 · The paper itself

Abstract

Akkermansia muciniphila (A. muciniphila), a beneficial gut bacterium, has increasingly attracted interests in Alzheimer's disease (AD) research, its specific role in the microbiota-gut-brain axis still remains unclear. In this study, we demonstrated that A. muciniphila administration improve cognitive deficits and reduce amyloid-beta (Aβ) deposition in APP/PS1 mice, a transgenic model of AD. Subsequently, it is revealed that A. muciniphila administration significantly alters gut microbiota diversity and composition. Mechanically, our metabolomics analysis of cecal contents indicates A. muciniphila administration increases short-chain fatty acids (SCFAs) derived from the intestinal microbiota, including butyric acid and acetic acid. Significantly, in APP/PS1 mice with the A. muciniphila administration, targeted metabolomics identify that the production of 62 metabolites are increased such as indole-3-acetic acid (IAA), tryptophan, acetic acid and cinnamic acid, as well as aconitic acid and threonine, et al.; the production of 28 metabolites are decreased such as isoleucine and N-acetylneuraminic acid (NANA) as well as ornithine and docosapentaenoic acid (DPA), et al. It is also identified by cytokine analysis of plasma that A. muciniphila administration reduces peripheral pro-inflammatory cytokines interleukin-6 (IL-6), IL-1β, IL-17 and tumor necrosis factor-alpha (TNF-α), et al., whereas it increases anti-inflammatory cytokines, such as IL-4, IL-10 and IL-22, et al. There is no any change of other cytokines, such as interferon-gamma (IFN-g), IL-2 and granulocyte-macrophage colony-stimulating factor (GM-CSF), et al. Interestingly, a significant positive correlation is observed between the increased IAA, tryptophan as well as acetic acid and cognitive function indicators. At the same time, A. muciniphila administration improves cognitive deficits, alleviates neuroinflammation and Aβ deposition via AhR/NF-κB/NLRP3 signaling pathway in APP/PS1 mice. In summary, our findings suggest A. muciniphila is a promising approach for preventing AD progression by microbiota-gut-brain axis.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesNeuroinflammatory DiseasesTryptophanAkkermansiaAmyloid beta-Protein PrecursorAnimalsDisease Models, AnimalGastrointestinal MicrobiomeMaleMiceMice, TransgenicAmyloid beta-PeptidesAmyloid beta-Protein PrecursorTryptophanAhR/NF-κB/NLRP3Akkermansia muciniphilaAlzheimer’s diseaseAmyloid betaCognitive deficitsGut microbiotaNeuroinflammationPeripheral inflammationTryptophan metabolism

Identifiers

PMID41715194
PMCPMC12922204

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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.