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REVIEW article

Front. Psychiatry

Sec. Autism

Volume 16 - 2025 | doi: 10.3389/fpsyt.2025.1587432

A Comprehensive Review of GABA in Autism Spectrum Disorders: Associations, Mechanisms, and Therapeutic implications

Provisionally accepted
Peng  WangPeng Wang1Jin  SunJin Sun2*
  • 1Department of graduate school, Dalian Medical University, Dalian, China
  • 2Department of Children's Health Medicine, Dalian Women and Children’s Medical Center(Group), Dalian, Liaoning Province, China

The final, formatted version of the article will be published soon.

The etiology and pathogenesis of Autism Spectrum Disorder (ASD) are not yet clear. Gamma-aminobutyric acid (GABA), as an inhibitory neurotransmitter in the brain, is closely related to the pathogenesis of ASD. Animal models and clinical studies of ASD suggest that abnormalities in GABAergic neurons, signaling pathways, and related genes may play an important role in the pathogenesis of ASD, leading to abnormal levels of GABA in the blood and brain tissue of individuals with ASD. Additionally, GABAergic drugs have shown potential to improve ASD symptoms in animal models, but their efficacy and safety in clinical use still need further research. Therefore, this article reviews the relationship between GABA and ASD, as well as the related research on GABA levels and drug treatment, to further explore the pathogenesis of ASD and provide a theoretical basis for the diagnosis and treatment.

Keywords: autism, GABA, GABAergic Neurons, GABAergic Drugs, GABA levels

Received: 05 Mar 2025; Accepted: 17 Sep 2025.

Copyright: © 2025 Wang and Sun. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Jin Sun, 916054417@qq.com

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