Does Dysbiosis Increase the Risk of Developing Schizophrenia? - A Comprehensive Narrative Review

失调 精神分裂症(面向对象编程) 疾病 肠道菌群 医学 叙述性评论 风险因素 生物信息学 免疫学 生物 精神科 重症监护医学 内科学
作者
Filipa Novais,Joana Capela,Sérgio Machado,Eric Murillo‐Rodríguez,Diogo Telles‐Correia
出处
期刊:Current Topics in Medicinal Chemistry [Bentham Science]
卷期号:21 (11): 976-984 被引量:2
标识
DOI:10.2174/1568026621666210521163555
摘要

Background: There is increasing evidence regarding the influence of the intestinal microbiota on the disease processes of various organs and systems. Dysbiosis, that is, alteration of the composition and function of the microbiota may constitute an important risk factor for the development of mental disorders, namely, schizophrenia. Objective: This works aims to review current evidence regarding the pathological mechanisms leading from dysbiosis to schizophrenia and in particular the deficit syndrome in schizophrenia. Methods: Scientific articles from PubMed, SCOPUS, EMBASE, and Web of Science Core Collection published between September 2017 and December 2020 were included in this review. Results: The commensal intestinal flora plays an important role in neurodevelopment. In the presence of dysbiosis, this maturation gets disturbed, resulting in the modification of brain structures and inflammatory responses at the intestinal, systemic, and Central Nervous System (CNS) levels. These disturbances may be linked to the development of symptoms of the disease. The microbiota exerts its influence on the CNS through several pathways, however, in this paper we focused on the membrane hypothesis and the inflammatory hypothesis. We explored the evidence concerning the use of probiotics, prebiotics, and fecal transplants. Conclusion: Although there is no consensus regarding the alterations that could constitute a risk factor for schizophrenia, some of the species appear to be more frequently altered, and their relationship with the host is dysregulated in patients at risk and with established schizophrenia, particularly in deficit schizophrenia.
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