Role of the gut microbiota in the pathophysiology of autism spectrum disorder: Clinical and preclinical evidence

L. Roussin, N. Prince, P. Perez-Pardo, A.D. Kraneveld, S. Rabot, L. Naudon

Research output: Contribution to JournalReview articleAcademicpeer-review

Abstract

© 2020 by the authors. Licensee MDPI, Basel, Switzerland.Autism spectrum disorder (ASD) is a neurodevelopmental disorder affecting 1 in 160 people in the world. Although there is a strong genetic heritability to ASD, it is now accepted that environmental factors can play a role in its onset. As the prevalence of gastrointestinal (GI) symptoms is four-times higher in ASD patients, the potential implication of the gut microbiota in this disorder is being increasingly studied. A disturbed microbiota composition has been demonstrated in ASD patients, accompanied by altered production of bacterial metabolites. Clinical studies as well as preclinical studies conducted in rodents have started to investigate the physiological functions that gut microbiota might disturb and thus underlie the pathophysiology of ASD. The first data support an involvement of the immune system and tryptophan metabolism, both in the gut and central nervous system. In addition, a few clinical studies and a larger number of preclinical studies found that modulation of the microbiota through antibiotic and probiotic treatments, or fecal microbiota transplantation, could improve behavior. Although the understanding of the role of the gut microbiota in the physiopathology of ASD is only in its early stages, the data gathered in this review highlight that this role should be taken in consideration.
Original languageEnglish
Article number1369
Pages (from-to)1-26
JournalMicroorganisms
Volume8
Issue number9
DOIs
Publication statusPublished - 1 Sept 2020
Externally publishedYes

Funding

This review was written in the context of the GEMMA project, funded by the European Commission by means of the Horizon 2020 program (call H2020-SC1-BHC-03-2018) with the project ID 825033.

FundersFunder number
H2020-SC1-BHC-03-2018

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