Evidence map›Paper›PMID 39833898›Full record

ArticleMicrobiome2025

Akkermansia muciniphila and its metabolite propionic acid maintains neuronal mitochondrial division and autophagy homeostasis during Alzheimer's disease pathologic process via GPR41 and GPR43.

Zifan Wang, Cai Wang, Boyu Yuan, Li Liu, Haoming Zhang, Mingqiang Zhu, Hongxia Chai, Jie Peng, Yanhua Huang, Shuo Zhou and 3 more

Abstract read
In one paragraph

Article in Microbiome, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 1 pooled it
–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

63 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Gut microbes · 2026
    Article
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  20. Biomolecules · 2026
    Review

3 more citing papers are in PubMed but not listed here.

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.

Zifan Wang *Innovative Institute of Animal Health Breeding, College of Animal Sciences and Technology, Zhongkai University of Agriculture and Engineering, Guangdong Province, Guangzhou, 510025, China.
Cai Wang *Internal Medicine Ward, Zhanlan Road Hospital, Xicheng District, Beijing, 100044, China.
Boyu Yuan *Department of Biochemistry, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, China.
Li Liu *Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, 100053, China.
Haoming ZhangInnovative Institute of Animal Health Breeding, College of Animal Sciences and Technology, Zhongkai University of Agriculture and Engineering, Guangdong Province, Guangzhou, 510025, China.
Mingqiang ZhuInnovative Institute of Animal Health Breeding, College of Animal Sciences and Technology, Zhongkai University of Agriculture and Engineering, Guangdong Province, Guangzhou, 510025, China.
Hongxia ChaiInnovative Institute of Animal Health Breeding, College of Animal Sciences and Technology, Zhongkai University of Agriculture and Engineering, Guangdong Province, Guangzhou, 510025, China.
Jie PengInnovative Institute of Animal Health Breeding, College of Animal Sciences and Technology, Zhongkai University of Agriculture and Engineering, Guangdong Province, Guangzhou, 510025, China.
Yanhua HuangInnovative Institute of Animal Health Breeding, College of Animal Sciences and Technology, Zhongkai University of Agriculture and Engineering, Guangdong Province, Guangzhou, 510025, China.
Shuo ZhouInnovative Institute of Animal Health Breeding, College of Animal Sciences and Technology, Zhongkai University of Agriculture and Engineering, Guangdong Province, Guangzhou, 510025, China.
Juxiong LiuKey Laboratory of Zoonoses Research, Ministry of Education, Jilin University, Changchun, 130062, China. juxiong@jlu.edu.cn.
Liyong WuDepartment of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, 100053, China. wmywly@hotmail.com.
Wei WangInnovative Institute of Animal Health Breeding, College of Animal Sciences and Technology, Zhongkai University of Agriculture and Engineering, Guangdong Province, Guangzhou, 510025, China. wang_wei99@jlu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlzheimer's disease (AD) is a prevalent neurodegenerative disease (ND). In recent years, multiple clinical and animal studies have shown that mitochondrial dysfunction may be involved in the pathogenesis of AD. In addition, short-chain fatty acids (SCFA) produced by intestinal microbiota metabolism have been considered to be important factors affecting central nervous system (CNS) homeostasis. Among the main mediators of host-microbe interactions, volatile fatty acids play a crucial role. Nevertheless, the influence and pathways of microorganisms and their metabolites on Alzheimer's disease (AD) remain uncertain.

resultsIn this study, we present distinctions in blood and fecal SCFA levels and microbiota composition between healthy individuals and those diagnosed with AD. We found that AD patients showed a decrease in the abundance of Akkermansia muciniphila and a decrease in propionic acid both in fecal and in blood. In order to further reveal the effects and the mechanisms of propionic acid on AD prevention, we systematically explored the effects of propionic acid administration on AD model mice and cultured hippocampal neuronal cells. Results showed that oral propionate supplementation ameliorated cognitive impairment in AD mice. Propionate downregulated mitochondrial fission protein (DRP1) via G-protein coupled receptor 41 (GPR41) and enhanced PINK1/PARKIN-mediated mitophagy via G-protein coupled receptor 43 (GPR43) in AD pathophysiology which contribute to maintaining mitochondrial homeostasis both in vivo and in vitro. Administered A. muciniphila to AD mice before disease onset showed improved cognition, mitochondrial division and mitophagy in AD mice.

conclusionsTaken together, our results demonstrate that A. muciniphila and its metabolite propionate protect against AD-like pathological events in AD mouse models by targeting mitochondrial homeostasis, making them promising therapeutic candidates for the prevention and treatment of AD. Video Abstract.

Indexed as

Alzheimer DiseaseAutophagyMitochondriaNeuronsPropionatesReceptors, G-Protein-CoupledVerrucomicrobiaAgedAkkermansiaAnimalsDisease Models, AnimalFatty Acids, VolatileFecesFemaleGastrointestinal MicrobiomeHippocampusFatty Acids, VolatileFfar2 protein, mousePropionatespropionic acidReceptors, G-Protein-CoupledAkkermansia muciniphilaAlzheimer’s diseaseMitochondrial division and mitophagyPropionic acid

Identifiers

PMID39833898
PMCPMC11744907

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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 Socratic graph.