Impaired blood‐brain barrier in the microbiota‐gut‐brain axis: Potential role of bipolar susceptibility gene <i>TRANK1</i>

Lai, Jianbo; Jiang, Jiajun; Zhang, Peifen; Xi, Caixi; Wu, Lingling; Gao, Xichao; Fu, Yaoyang; Chen, Yiqing; Huang, Huimin; Zhu, Yiyi; Hu, Shaohua

doi:10.1111/jcmm.16611

Cited by 10 publications

(4 citation statements)

References 62 publications

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“…The BBB regulates brain physiology by maintaining chemical and nutritional exchanges [156]. Preclinical [157] and clinical studies [158] have revealed that disruption in the BBB can lead to behavioral and memory deficits.…”

Section: Sa-related Gd and Cognitive Declinementioning

confidence: 99%

Sleep apnoea, gut dysbiosis and cognitive dysfunction

Deyang,

Baig,

Dolkar

et al. 2023

The FEBS Journal

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Sleep disorders are becoming increasingly common, and their distinct effects on physical and mental health require elaborate investigation. Gut dysbiosis (GD) has been reported in sleep‐related disorders, but sleep apnoea is of particular significance because of its higher prevalence and chronicity. Cumulative evidence has suggested a link between sleep apnoea and GD. This Review highlights the gut–brain communication axis that is mediated via commensal microbes and various microbiota‐derived metabolites [such as short‐chain fatty acids (SCFAs), lipopolysaccharide (LPS) and trimethyl amine N‐oxide (TMAO)], neurotransmitters (such as γ‐aminobutyric acid, serotonin, glutamate, and dopamine), immune cells and inflammatory mediators, as well as the vagus nerve and hypothalamic–pituitary–adrenal (HPA) axis. This Review also discusses the pathological role underpinning GD and altered gut bacterial populations in sleep apnoea and its related comorbid conditions, particularly cognitive dysfunction. The Review also examines the preclinical and clinical evidence, which suggests that prebiotics and probiotics may potentially be beneficial in sleep apnoea and its comorbidities through restoration of eubiosis or gut microbial homeostasis that regulates neural, metabolic, and immune responses, as well as physiological barrier integrity via the gut–brain axis.

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Section: Sa-related Gd and Cognitive Declinementioning

confidence: 99%

Sleep apnoea, gut dysbiosis and cognitive dysfunction

Deyang,

Baig,

Dolkar

et al. 2023

The FEBS Journal

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“…This conclusion is mainly based on animal studies [ 60 , 75 ]. However, some studies in humans have also indicated that gut microbiota may affect BBB function [ 108 ]. The panicogenic substances released during meals may then reach their receptors in the brain and induce anxiety when a susceptible malnourished individual starts eating.…”

Section: The Gut Microbiota–brain Axis and Anorexia Nervosamentioning

confidence: 99%

Are the Effects of Malnutrition on the Gut Microbiota–Brain Axis the Core Pathologies of Anorexia Nervosa?

Frostad

2022

Microorganisms

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Anorexia nervosa (AN) is a disabling, costly, and potentially deadly illness. Treatment failure and relapse after treatment are common. Several studies have indicated the involvement of the gut microbiota–brain (GMB) axis. This narrative review hypothesizes that AN is driven by malnutrition-induced alterations in the GMB axis in susceptible individuals. According to this hypothesis, initial weight loss can voluntarily occur through dieting or be caused by somatic or psychiatric diseases. Malnutrition-induced alterations in gut microbiota may increase the sensitivity to anxiety-inducing gastrointestinal hormones released during meals, one of which is cholecystokinin (CCK). The experimental injection of a high dose of its CCK-4 fragment in healthy individuals induces panic attacks, probably via the stimulation of CCK receptors in the brain. Such meal-related anxiety attacks may take part in developing the clinical picture of AN. Malnutrition may also cause increased effects from appetite-reducing hormones that also seem to have roles in AN development and maintenance. The scientific background, including clinical, microbiological, and biochemical factors, of AN is discussed. A novel model for AN development and maintenance in accordance with this hypothesis is presented. Suggestions for future research are also provided.

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“…Interestingly, a negative correlation between gut microbial diversity and methylation of the aryl hydrocarbon receptor nuclear translocator-like gene (ARNTL), a molecular clock gene linked to circadian rhythm, was revealed in BD patients (13). In our recent review, we have systematically discussed a hypothesis that gut microbe-derived LPS could influence the host TRNAK1 expression in BD (14). These preliminary findings indicate the involvement of the microbiota-gut-brain regulation in BD.…”

Section: Introductionmentioning

confidence: 99%

New Evidence of Gut Microbiota Involvement in the Neuropathogenesis of Bipolar Depression by TRANK1 Modulation: Joint Clinical and Animal Data

et al. 2021

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Tetratricopeptide repeat and ankyrin repeat containing 1 (TRANK1) is a robust risk gene of bipolar disorder (BD). However, little is known on the role of TRANK1 in the pathogenesis of BD and whether the gut microbiota is capable of regulating TRANK1 expression. In this study, we first investigated the serum mRNA level of TRANK1 in medication-free patients with a depressive episode of BD, then a mice model was constructed by fecal microbiota transplantation (FMT) to explore the effects of gut microbiota on brain TRANK1 expression and neuroinflammation, which was further verified by in vitro Lipopolysaccharide (LPS) treatment in BV-2 microglial cells and neurons. 22 patients with a depressive episode and 28 healthy individuals were recruited. Serum level of TRANK1 mRNA was higher in depressed patients than that of healthy controls. Mice harboring ‘BD microbiota’ following FMT presented depression-like phenotype. mRNA levels of inflammatory cytokines and TRANK1 were elevated in mice hippocampus and prefrontal cortex. In vitro, LPS treatment activated the secretion of pro-inflammatory factors in BV-2 cells, which was capable of upregulating the neuronal expression of TRANK1 mRNA. Moreover, primary cortical neurons transfected with plasmid Cytomegalovirus DNA (pcDNA3.1(+)) vector encoding human TRANK1 showed decreased dendritic spine density. Together, these findings add new evidence to the microbiota-gut-brain regulation in BD, indicating that microbiota is possibly involved in the neuropathogenesis of BD by modulating the expression of TRANK1.

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Impaired blood‐brain barrier in the microbiota‐gut‐brain axis: Potential role of bipolar susceptibility gene TRANK1

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 10 publications

References 62 publications

Sleep apnoea, gut dysbiosis and cognitive dysfunction

Sleep apnoea, gut dysbiosis and cognitive dysfunction

Are the Effects of Malnutrition on the Gut Microbiota–Brain Axis the Core Pathologies of Anorexia Nervosa?

New Evidence of Gut Microbiota Involvement in the Neuropathogenesis of Bipolar Depression by TRANK1 Modulation: Joint Clinical and Animal Data

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