Abstract

Schizophrenia is a severe neuropsychiatric disorder, and its etiology remains largely unknown. Environmental factors have been reported to play roles in the pathogenesis of schizophrenia, and one of the major environmental factors identified for this disorder is psychosocial stress. Several studies have suggested that stressful life events, as well as the chronic social stress associated with city life, may lead to the development of schizophrenia. The other factor is the gut–brain axis. The composition of the gut microbiome and alterations thereof may affect the brain and may lead to schizophrenia. The main interest of this review article is in overviewing the major recent findings on the effects of stress and the gut–brain axis, as well as their possible bidirectional effects, in the pathogenesis of schizophrenia.

Highlights

  • Around 792 million people in the world live with mental disorders, which is more than one in ten people (10.7%) globally [1]

  • The author aimed to bring together some recent studies that showed the effects of stress as well as dysregulation of the gut–brain axis on the pathogenesis of schizophrenia

  • There are several reports showing the symptoms of schizophrenia in patients or animal models after being exposed to environmental factors, such as stress, or models with dysregulations in the gut–brain axis

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Summary

Introduction

Around 792 million people in the world live with mental disorders, which is more than one in ten people (10.7%) globally [1]. There is increasing evidence that disorders such as schizophrenia are associated with an imbalance in the gut microbiome [5,6]. The effects of environmental factors (stress) together with those of the dysregulation of the gut–brain axis on the pathogenesis of schizophrenia will be discussed in this review (Figure 1). This can be interesting due to the fact that there are few studies that show the bidirectional effects of these factors.

Schizophrenia
Stress
Gut–Brain Axis
Stress and Gut Microbiome
Findings
Conclusions
Full Text
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