Evidence map›Paper›PMID 39093342›Full record

ReviewInflammation2025

Gut Microbiota and Autism Spectrum Disorder: A Neuroinflammatory Mediated Mechanism of Pathogenesis?

Fatemeh Zarimeidani, Rahem Rahmati, Mehrnaz Mostafavi, Mohammad Darvishi, Sanaz Khodadadi, Mahya Mohammadi, Farid Shamlou, Salar Bakhtiyari, Iraj Alipourfard

Abstract readReview
In one paragraph

Review in Inflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing 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

32 citing papers in PubMed.

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  6. A Developmental Neuroimmune Cascade Model of Autism Spectrum Disorder.International journal of molecular sciences · 2026
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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

9 authors.

Fatemeh Zarimeidani *Students Research Committee, Shahrekord University of Medical Sciences, Shahrekord, Iran.
Rahem Rahmati *Students Research Committee, Shahrekord University of Medical Sciences, Shahrekord, Iran.
Mehrnaz MostafaviFaculty of Allied Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Mohammad DarvishiSchool of Aerospace and Subaquatic Medicine, Infectious Diseases & Tropical Medicine Research Center (IDTMC), AJA University of Medical Sciences, Tehran, Iran.
Sanaz KhodadadiStudent Research Committee, Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran.
Mahya MohammadiStudent Research Committee, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Farid ShamlouSchool of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
Salar BakhtiyariFeinberg Cardiovascular and Renal Research Institute, North Western University, Chicago. Illinois, USA.
Iraj AlipourfardInstitute of Physical Chemistry, Polish Academy of Sciences, Marcin Kasprzaka 44/52, 01-224, Warsaw, Poland. ialipourfard@ichf.edu.pl.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by impairments in social communication and behavior, frequently accompanied by restricted and repetitive patterns of interests or activities. The gut microbiota has been implicated in the etiology of ASD due to its impact on the bidirectional communication pathway known as the gut-brain axis. However, the precise involvement of the gut microbiota in the causation of ASD is unclear. This study critically examines recent evidence to rationalize a probable mechanism in which gut microbiota symbiosis can induce neuroinflammation through intermediator cytokines and metabolites. To develop ASD, loss of the integrity of the intestinal barrier, activation of microglia, and dysregulation of neurotransmitters are caused by neural inflammatory factors. It has emphasized the potential role of neuroinflammatory intermediates linked to gut microbiota alterations in individuals with ASD. Specifically, cytokines like brain-derived neurotrophic factor, calprotectin, eotaxin, and some metabolites and microRNAs have been considered etiological biomarkers. We have also overviewed how probiotic trials may be used as a therapeutic strategy in ASD to reestablish a healthy balance in the gut microbiota. Evidence indicates neuroinflammation induced by dysregulated gut microbiota in ASD, yet there is little clarity based on analysis of the circulating immune profile. It deems the repair of microbiota load would lower inflammatory chaos in the GI tract, correct neuroinflammatory mediators, and modulate the neurotransmitters to attenuate autism. The interaction between the gut and the brain, along with alterations in microbiota and neuroinflammatory biomarkers, serves as a foundational background for understanding the etiology, diagnosis, prognosis, and treatment of autism spectrum disorder.

Indexed as

Autism Spectrum DisorderGastrointestinal MicrobiomeNeuroinflammatory DiseasesAnimalsBrainBrain-Gut AxisHumansProbioticsautism spectrum disorderbiomarkergut microbiotainflammationneuroinflammation

Identifiers

PMID39093342
PMCPMC12053372

What Socratic holds

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LicenceCC BY
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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.