Format

Send to

Choose Destination
Curr Neurol Neurosci Rep. 2018 Sep 24;18(11):81. doi: 10.1007/s11910-018-0887-6.

The Gut Microbiota and Dysbiosis in Autism Spectrum Disorders.

Author information

1
Department of Medical Microbiology and Immunology, UC Davis, 2805, 50th Street, Sacramento, CA, 95817, USA.
2
The M.I.N.D. Institute, University of California at Davis, Davis, CA, USA.
3
Department of Medical Microbiology and Immunology, UC Davis, 2805, 50th Street, Sacramento, CA, 95817, USA. pashwood@ucdavis.edu.
4
The M.I.N.D. Institute, University of California at Davis, Davis, CA, USA. pashwood@ucdavis.edu.

Abstract

PURPOSE OF REVIEW:

There is a growing body of evidence indicating the gut microbiota influence neurodevelopment and behavior. The purposes of this review are to provide an overview of studies analyzing the microbiota and their metabolites in autism spectrum disorders (ASD) and to discuss the possible mechanisms of action involved in microbial influence on the brain and behavior.

RECENT FINDINGS:

The microbiota-gut-brain (MGB) axis has been extensively studied in animal models, and it is clear that alterations in the composition of microbiota alter neurological and behavioral outcomes. However, findings in human studies are less abundant. Although there are several studies so far showing altered microbiota (dysbiosis) in ASD, the results are heterogeneous and often contradictory. Intervention studies such as fecal microbiota transplant therapies show promise and lend credence to the involvement of the microbiota in ASD. A role for the microbiota in ASD is likely; however, further studies elucidating microbial or metabolomic signatures and mechanisms of action are needed. Future research should focus on intervention studies that can identify specific metabolites and immune mediators that improve with treatment to help identify etiologies and pathological mechanisms of ASD.

KEYWORDS:

Autism; Behavior; Dysbiosis; Dysregulation; Microbiota; Neurodevelopment

PMID:
30251184
DOI:
10.1007/s11910-018-0887-6

Supplemental Content

Full text links

Icon for Springer
Loading ...
Support Center