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自闭症中脑-肠轴的改变:共病还是致病机制?

Altered brain-gut axis in autism: comorbidity or causative mechanisms?

作者信息

Mayer Emeran A, Padua David, Tillisch Kirsten

机构信息

Oppenheimer Center for Neurobiology of Stress, Division of Digestive Diseases, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.

出版信息

Bioessays. 2014 Oct;36(10):933-9. doi: 10.1002/bies.201400075. Epub 2014 Aug 22.

Abstract

The concept that alterated communications between the gut microbiome and the brain may play an important role in human brain disorders has recently received considerable attention. This is the result of provocative preclinical and some clinical evidence supporting early hypotheses about such communication in health and disease. Gastrointestinal symptoms are a common comorbidity in patients with autism spectrum disorders (ASD), even though the underlying mechanisms are largely unknown. In addition, alteration in the composition and metabolic products of the gut microbiome has long been implicated as a possible causative mechanism contributing to ASD pathophysiology, and this hypothesis has been supported by several recently published evidence from rodent models of autism induced by prenatal insults to the mother. Recent evidence in one such model involving maternal infection, that is characterized by alterations in behavior, gut physiology, microbial composition, and related metabolite profile, suggests a possible benefit of probiotic treatment on several of the observed abnormal behaviors.

摘要

肠道微生物群与大脑之间的交流改变可能在人类脑部疾病中起重要作用,这一概念最近受到了相当多的关注。这是有启发性的临床前研究以及一些临床证据的结果,这些证据支持了关于健康和疾病中这种交流的早期假设。胃肠道症状是自闭症谱系障碍(ASD)患者常见的合并症,尽管其潜在机制在很大程度上尚不清楚。此外,肠道微生物群的组成和代谢产物的改变长期以来一直被认为是导致ASD病理生理学的一种可能的致病机制,这一假设得到了最近发表的几篇关于产前母体受损伤诱导的自闭症啮齿动物模型的证据的支持。在一个涉及母体感染的此类模型中的最新证据表明,益生菌治疗可能对观察到的几种异常行为有益,该模型的特征是行为、肠道生理学、微生物组成和相关代谢物谱的改变。

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