Evidence map›Paper›PMID 41580690›Full record

ArticleJournal of nanobiotechnology2026

Akkermansia muciniphila vesicles attenuate smoking-induced cognitive decline via ILA-mediated AhR-dependent microglial reprogramming.

Bowen Zhu, Jiayuan Huang, Haoran Zhang, Hongqi Lin, Turi Chen, Ling Min, Yitian Yang, Youtan Liu, Songhe Guo

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of nanobiotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Review
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

9 authors.

Bowen Zhu *Department of Anesthesiology, Shenzhen Hospital, Southern Medical University, Shenzhen, 518101, China.
Jiayuan Huang *School of Medicine, Shenzhen Campus of Sun Yat-Sen University, Shenzhen, 518107, China.
Haoran Zhang *Department of Anesthesia, Department of Anesthesia of Central China Fu Wai Hospital, Zhengzhou University People's Hospital, Henan Provincial People's HospitalHenan Provincial People's HospitalCentral China Fu Wai Hospital of Zhengzhou University, Zhengzhou, 450003, China.
Hongqi LinDepartment of Anesthesia, Department of Anesthesia of Central China Fu Wai Hospital, Zhengzhou University People's Hospital, Henan Provincial People's HospitalHenan Provincial People's HospitalCentral China Fu Wai Hospital of Zhengzhou University, Zhengzhou, 450003, China.
Turi ChenGuangzhou Institute of Cancer Research, the Affiliated Cancer Hospital, Guangzhou Medical University, Guangzhou, 510095, China.
Ling MinGuangzhou Institute of Cancer Research, the Affiliated Cancer Hospital, Guangzhou Medical University, Guangzhou, 510095, China.
Yitian YangDepartment of Anesthesiology and Perioperative Medicine, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, Zhengzhou, 45000, China. yangyitiansdu@126.com.
Youtan LiuDepartment of Anesthesiology, Shenzhen Hospital, Southern Medical University, Shenzhen, 518101, China. youtanliuhao@163.com.
Songhe GuoGuangzhou Institute of Cancer Research, the Affiliated Cancer Hospital, Guangzhou Medical University, Guangzhou, 510095, China. 2025991009@gzhmu.edu.cn.

Funding

Guangdong Provincial Clinical Research Center for Laboratory Medicine 2023B110008Shenzhen Medical Research Fund A2402014Youth Foundation of the National Natural Science Foundation of China 32300761
6 · The paper itself

Abstract

Chronic cigarette smoking accelerates age-related cognitive decline, yet the underlying mechanism remains elusive. Here, we elucidate a pathway through which smoking-induced gut dysbiosis contributes to cognitive impairment. This dysbiosis is marked by reductions in the abundances of Akkermansia muciniphila (A. muciniphila) and its metabolite indole-3-lactic acid (ILA), which correlate with cognitive deficits in older adult smokers. Using fecal microbiota transplantation, we demonstrate that the microbiota from smoke-exposed donors recapitulates cognitive impairment and microglial dysfunction in recipient mice. Importantly, these deficits were mitigated by treatment with either A. muciniphila-derived outer membrane vesicles (OMVs) or exogenous ILA, which restore synaptic integrity. Mechanistically, we demonstrate that both OMVs and ILA exert their neuroprotective effects via aryl hydrocarbon receptor (AhR) signaling. This AhR-dependent activation reprograms microglial metabolism toward oxidative phosphorylation, thereby suppressing neuroinflammation and restoring cellular bioenergetics. These findings suggest a mechanism through which smoking influences brain function via specific gut microbial metabolites and highlight the A. muciniphila-ILA-AhR axis as a promising target for preventing cognitive decline.

Indexed as

Cognitive DysfunctionMicrogliaReceptors, Aryl HydrocarbonSmokingAkkermansiaAnimalsFecal Microbiota TransplantationGastrointestinal MicrobiomeHumansMaleMiceMice, Inbred C57BLSignal TransductionReceptors, Aryl HydrocarbonAkkermansia muciniphilaCognitive impairmentGut-brain axisIndole-3-lactic acid (ILA)NeuroinflammationOuter membrane vesicles (OMVs)

Identifiers

PMID41580690
PMCPMC12911188

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.