Evidence map›Paper›PMID 32819434›Full record

ArticleMicrobiome2020

The gut microbiota regulates autism-like behavior by mediating vitamin B

Ying Li, Zheng-Yi Luo, Yu-Ying Hu, Yue-Wei Bi, Jian-Ming Yang, Wen-Jun Zou, Yun-Long Song, Shi Li, Tong Shen, Shu-Ji Li and 4 more

Registry-linked trialOpen access · goldAbstract readVideo-Audio Media
In one paragraph

Article in Microbiome, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07546942 (Autism Spectral Disorder), which is not on this map. Cited by 72 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 1 pooled it
7.6field-weighted citation impact, top 2% 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.

NCT07546942 phase1 / phase2enrolling by invitationnot on this mapstarted 2026, after this paper: background citation

Autism Spectral Disorder (ASD) In Adolescent-Adults Treated by Multimodal Protocol: IV Autologous cSVF, Interval IV Autologous MSCs (Cryopreserved), Strick Ketogenic Diet RESET Program, and Fecal Microbiota Transplantation (FMT)

TypeinterventionalSponsorBlack Tie Medical, Inc.Ran2026 to 2030Enrolled50ConditionsAutism Spectrum Disorder, Autism, Autism Spectral DisorderArmsAutologous MSC isolation, concentration, and cryopreservation of adult mesenchymal stem cells, Fecal Biomicrome Transplantation (FMT), Ketogenic RESET Diet Protocol, Trial combines use of cSVF and MSCs (cryopres) with diet modification and FMT (fecal material Transplant in adult ASD patients, FMT (Fecal Material Tranplantation)
3 · Its place in the literature

Who cites it

72 citing papers in PubMed, 1 synthesis or guideline pooled it, 142 citations in OpenAlex.

  1. Pooled it
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  9. Association between serum vitamin BThe British journal of nutrition · 2026
    Article
  10. Observational
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  12. The Eph-ephrin system in neuropsychiatric and neurodevelopmental disorders.Journal of psychiatry & neuroscience : JPN · 2026
    Review
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12 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

14 authors at 4 institutions in 2 countries.

Ying LiDepartment of Pathology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, People's Republic of China.
Zheng-Yi LuoDepartment of Pathology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, People's Republic of China.
Yu-Ying HuDepartment of Pathology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, People's Republic of China.
Yue-Wei BiState Key Laboratory of Organ Failure Research, Key Laboratory of Mental Health of the Ministry of Education, Guangdong-Hong Kong-Macao Greater Bay Area Center for Brain Science and Brain-Inspired Intelligence, Guangdong Province Key Laboratory of Psychiatric Disorders Collaborative Innovation Center for Brain Science, Department of Neurobiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, People's Republic of China.
Jian-Ming YangState Key Laboratory of Organ Failure Research, Key Laboratory of Mental Health of the Ministry of Education, Guangdong-Hong Kong-Macao Greater Bay Area Center for Brain Science and Brain-Inspired Intelligence, Guangdong Province Key Laboratory of Psychiatric Disorders Collaborative Innovation Center for Brain Science, Department of Neurobiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, People's Republic of China.
Wen-Jun ZouState Key Laboratory of Organ Failure Research, Key Laboratory of Mental Health of the Ministry of Education, Guangdong-Hong Kong-Macao Greater Bay Area Center for Brain Science and Brain-Inspired Intelligence, Guangdong Province Key Laboratory of Psychiatric Disorders Collaborative Innovation Center for Brain Science, Department of Neurobiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, People's Republic of China.
Yun-Long SongState Key Laboratory of Organ Failure Research, Key Laboratory of Mental Health of the Ministry of Education, Guangdong-Hong Kong-Macao Greater Bay Area Center for Brain Science and Brain-Inspired Intelligence, Guangdong Province Key Laboratory of Psychiatric Disorders Collaborative Innovation Center for Brain Science, Department of Neurobiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, People's Republic of China.
Shi LiDepartment of Pathology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, People's Republic of China.
Tong ShenDepartment of Pathology, Soochow University Medical School, Suzhou, 215123, People's Republic of China.
Shu-Ji LiState Key Laboratory of Organ Failure Research, Key Laboratory of Mental Health of the Ministry of Education, Guangdong-Hong Kong-Macao Greater Bay Area Center for Brain Science and Brain-Inspired Intelligence, Guangdong Province Key Laboratory of Psychiatric Disorders Collaborative Innovation Center for Brain Science, Department of Neurobiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, People's Republic of China.
Lang HuangState Key Laboratory of Organ Failure Research, Key Laboratory of Mental Health of the Ministry of Education, Guangdong-Hong Kong-Macao Greater Bay Area Center for Brain Science and Brain-Inspired Intelligence, Guangdong Province Key Laboratory of Psychiatric Disorders Collaborative Innovation Center for Brain Science, Department of Neurobiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, People's Republic of China.
Ai-Jun ZhouDepartment of Pathology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, People's Republic of China.
Tian-Ming GaoState Key Laboratory of Organ Failure Research, Key Laboratory of Mental Health of the Ministry of Education, Guangdong-Hong Kong-Macao Greater Bay Area Center for Brain Science and Brain-Inspired Intelligence, Guangdong Province Key Laboratory of Psychiatric Disorders Collaborative Innovation Center for Brain Science, Department of Neurobiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, People's Republic of China. tgao@smu.edu.cn.
Jian-Ming LiDepartment of Pathology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, People's Republic of China. lijming3@sysu.edu.cn.ORCID 0000-0002-7999-2385
Sun Yat-sen University · CNSouthern Medical University · CNMinistry of Education · RWSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAutism spectrum disorder (ASD) is a developmental disorder, and the effective pharmacological treatments for the core autistic symptoms are currently limited. Increasing evidence, particularly that from clinical studies on ASD patients, suggests a functional link between the gut microbiota and the development of ASD. However, the mechanisms linking the gut microbiota with brain dysfunctions (gut-brain axis) in ASD have not yet been full elucidated. Due to its genetic mutations and downregulated expression in patients with ASD, EPHB6, which also plays important roles in gut homeostasis, is generally considered a candidate gene for ASD. Nonetheless, the role and mechanism of EPHB6 in regulating the gut microbiota and the development of ASD are unclear.

resultsHere, we found that the deletion of EphB6 induced autism-like behavior and disturbed the gut microbiota in mice. More importantly, transplantation of the fecal microbiota from EphB6-deficient mice resulted in autism-like behavior in antibiotic-treated C57BL/6J mice, and transplantation of the fecal microbiota from wild-type mice ameliorated the autism-like behavior in EphB6-deficient mice. At the metabolic level, the disturbed gut microbiota in EphB6-deficient mice led to vitamin B

conclusionsOur study uncovers a key role for the gut microbiota in the regulation of autism-like social behavior by vitamin B

Indexed as

Gastrointestinal MicrobiomeHomeostasisAnimalsAutism Spectrum DisorderAutistic DisorderDopamineMaleMiceMice, Inbred C57BLNeural InhibitionPrefrontal CortexReceptors, Eph FamilySocial BehaviorVitamin B 6DopamineEPHB6 protein, humanReceptors, Eph FamilyVitamin B 6ASDDopamineE/I balanceEphB6Gut microbiotaVitamin B6

Identifiers

PMID32819434
PMCPMC7441571
OpenAlexW3068244390

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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.