Microbiota–Gut–Brain Axis: Pathophysiological Mechanism in Neuropsychiatric Disorders

  • Cheolmin Shin
  • , Yong Ku Kim*
  • *Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Gut microbiota influence human behavior. The immunological, metabolic, and endocrine systems are involved in bidirectional communication between the gut and the brain, which is regulated by microbes through the microbiota-derived neurochemicals and metabolites. Gut microbiota have certain effects on neurodevelopment and maturation of immunity. However, gut dysbiosis can lead to neuropsychiatric disorders. Animal research and clinical case-control studies have demonstrated that gut dysbiosis has an adverse effect on human behavior through a variety of mechanisms. Recent meta-analysis on clinical studies confirmed gut dysbiosis in several major neuropsychiatric disorders. Microbiota-targeted intervention has recently been in the spotlight and meta-analyses have confirmed its effectiveness. In this chapter, we summarize the evidence for the interactions between microbiota and brain–gut network, as well as the potential pathophysiological mechanisms involved.

Original languageEnglish
Title of host publicationAdvances in Experimental Medicine and Biology
PublisherSpringer
Pages17-37
Number of pages21
DOIs
Publication statusPublished - 2023

Publication series

NameAdvances in Experimental Medicine and Biology
Volume1411
ISSN (Print)0065-2598
ISSN (Electronic)2214-8019

Bibliographical note

Publisher Copyright:
© 2023, The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd.

Keywords

  • Fecal microbiota transplantation
  • Gut-dysbiosis
  • Microbiota
  • Microbiota–gut–brain axis
  • Probiotics

ASJC Scopus subject areas

  • General Biochemistry,Genetics and Molecular Biology

Fingerprint

Dive into the research topics of 'Microbiota–Gut–Brain Axis: Pathophysiological Mechanism in Neuropsychiatric Disorders'. Together they form a unique fingerprint.

Cite this