Evidence map›Paper›PMID 39809266›Full record

ArticleCell reports. Medicine2025

Gut microbial GABA imbalance emerges as a metabolic signature in mild autism spectrum disorder linked to overrepresented Escherichia.

Dilong Wang, Youheng Jiang, Jian Jiang, Yihang Pan, Yanming Yang, Xiaoyi Fang, Liyang Liang, Hai Li, Zepeng Dong, Shilu Fan and 5 more

Abstract read
In one paragraph

Article in Cell reports. Medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing 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

33 citing papers in PubMed.

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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

15 authors.

Dilong WangTomas Lindahl Nobel Laureate Laboratory, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong 518107, China; Department of Pediatrics, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510000, China.
Youheng JiangTomas Lindahl Nobel Laureate Laboratory, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong 518107, China; Center for Digestive Disease, Guangdong Provincial Key Laboratory of Digestive Cancer Research, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong 518107, China.
Jian JiangTomas Lindahl Nobel Laureate Laboratory, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong 518107, China; Center for Clinical Molecular Medicine, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University, Chongqing 400014, China.
Yihang PanTomas Lindahl Nobel Laureate Laboratory, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong 518107, China; Center for Digestive Disease, Guangdong Provincial Key Laboratory of Digestive Cancer Research, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong 518107, China.
Yanming YangTomas Lindahl Nobel Laureate Laboratory, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong 518107, China.
Xiaoyi FangDepartment of Neonatology, The Seventh Affiliated Hospital of Sun Yat-sen University, Shenzhen, Guangdong 518107, China.
Liyang LiangDepartment of Pediatrics, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510000, China.
Hai LiNeurorehabilitation Laboratory, Department of Rehabilitation Medicine, Shenzhen Hospital, Shenzhen, Guangdong 518107, China.
Zepeng DongTomas Lindahl Nobel Laureate Laboratory, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong 518107, China.
Shilu FanARK Autism & Rehabilitation Institute, Taiyuan, Shanxi 030000, China.
Daqing MaDivision of Anaesthetics, Pain Medicine and Intensive Care, Imperial College London, Chelsea and Westminster Hospital, London SW10 9NH, UK; Perioperative and Systems Medicine Laboratory, Children's Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China.
Xue-Song ZhangCenter for Advanced Biotechnology and Medicine, Rutgers University, Piscataway, NJ 08854, USA. Electronic address: xuesong.zhang@rutgers.edu.
Huiliang LiWolfson Institute for Biomedical Research, Division of Medicine, Faculty of Medical Sciences, University College London, London WC1E 6AE, UK. Electronic address: huiliang.li@ucl.ac.uk.
Yulong HeTomas Lindahl Nobel Laureate Laboratory, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong 518107, China; Center for Digestive Disease, Guangdong Provincial Key Laboratory of Digestive Cancer Research, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong 518107, China. Electronic address: heyulong@mail.sysu.edu.cn.
Ningning LiTomas Lindahl Nobel Laureate Laboratory, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong 518107, China; China-UK Institute for Frontier Science, Shenzhen 518107, China. Electronic address: linn29@mail.sysu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gut microbiota (GM) alterations have been implicated in autism spectrum disorder (ASD), yet the specific functional architecture remains elusive. Here, employing multi-omics approaches, we investigate stool samples from two distinct cohorts comprising 203 children with mild ASD or typical development. In our screening cohort, regression-based analysis for metabolomic profiling identifies an elevated γ-aminobutyric acid (GABA) to glutamate (Glu) ratio as a metabolic signature of ASD, independent of age and gender. In the validating cohort, we affirm the GABA/Glu ratio as an ASD diagnostic indicator after adjusting for geography, age, gender, and specific food-consuming frequency. Integrated analysis of metabolomics, 16S rRNA sequencing, and metagenomics reveals a correlation between overrepresented Escherichia and disrupted GABA metabolism. Furthermore, we observe social behavioral impairments in weaning mice transplanted with E. coli, suggesting a potential link to ASD symptomatology. Collectively, these findings provide insights into potential diagnostic and therapeutic strategies aimed at evaluating and restoring gut microbial neurotransmitter homeostasis.

Indexed as

Autism Spectrum DisorderEscherichia coligamma-Aminobutyric AcidGastrointestinal MicrobiomeAdolescentAnimalsChildChild, PreschoolFecesFemaleGlutamic AcidHumansMaleMetabolomeMetabolomicsMicegamma-Aminobutyric AcidGlutamic AcidRNA, Ribosomal, 16Sautismdiagnostic biomarkerEscherichiaglutamategut-brain axisgut microbiotametabolomemulti-omicsneurotransmitter homeostasisγ-aminobutyric acid

Identifiers

PMID39809266
PMCPMC11866488

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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.