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[Microbe-gut-brain axis and neurological disorders: a review].
Intestinal microbes have an adjuvant therapeutic effect on neurological disorders (such as Parkinson's, depression, and Alzheimer's disease). It affects brain function and host behavior through the neural pathways, the immune pathways and the microbial metabolites, the so-called gut-brain axis. This article summarizes the recent advances in the role of the microbe-gut-brain axis in neurological disorders, in order to provide new ideas for the treatment of neurodegenerative diseases.
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Lycopene regulates intestinal dysmotility and behavioral disorders by regulating enteric neurons and the cholinergic system.
Gut dysmotility is a prevalent gastrointestinal disorder characterized by disrupted defecation and often accompanied by depression and anxiety. Lycopene (LYC) is a type of carotenoid with strong antioxidant and anti-inflammatory properties. However, the effects of LYC on gut dysmotility and related behavioral disorders remain elusive. Herein, we found that 100 mg kg-1 d-1 LYC notably improved the gut transit time and intestinal transit rate as well as concurrently alleviated depression- and anxiety-like behaviors in a diphenoxylate (Dip, 5 mg kg-1 d-1)-induced constipated mouse model. LYC pretreatment enhanced gut barrier integrity and short-chain fatty acid (SCFA) production as well as rebalanced gut microbiota homeostasis by enriching beneficial bacteria, including Bifidobacterium and Akkermansia. Furthermore, LYC restored enteric neuronal function, as evidenced by increased HuC/D and Tuj1 expression as well as balanced neurotransmitter levels. Brain transcriptomics results suggest that LYC regulates the cholinergic synapse pathway and increases acetylcholine (Ach) content in the brain, which is associated with the alleviation of neuroinflammation. In summary, this study offers insights into functional dietary component-based nutritional strategies that target gut dysmotility comorbid behavioral dysfunction.
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Impact of Microbiota on Irritable Bowel Syndrome Pathogenesis and Management: A Narrative Review.
Irritable bowel syndrome (IBS) is a prevalent gastrointestinal disorder, affecting 3-5% of the global population and significantly impacting patients' quality of life and healthcare resources. Alongside physical symptoms such as abdominal pain and altered bowel habits, many individuals experience psychological comorbidities, including anxiety and depression. Recent research has highlighted the critical role of the gut microbiota in IBS, with dysbiosis, characterized by an imbalance in microbial diversity, frequently observed in patients. The gut-brain axis, a bidirectional communication network between the gut and central nervous system, plays a central role in the development of IBS symptoms. Although interventions such as probiotics, prebiotics, synbiotics, and fecal microbiota transplantation (FMT) have demonstrated potential in modulating the gut microbiota and alleviating symptoms, their efficacy remains an area of ongoing investigation. This review examines the interactions between the gut microbiota, immune system, and brain, emphasizing the need for personalized therapeutic strategies. Future research should aim to identify reliable microbiota-based biomarkers for IBS and refine microbiome-targeted therapies to enhance patient outcomes.
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Protocol for a pilot feasibility randomised controlled trial of fecal microbiota transplantation for adolescent anorexia nervosa.
INTRODUCTION: Despite its serious impact, anorexia nervosa (AN) remains one of the least understood mental illnesses, with significant gaps in effective treatment options. No medications have been deemed effective and only 50% of individuals respond to conventional psychotherapies. Gastrointestinal (GI) bacteria have been found to be altered in individuals with AN. While, Fecal microbiota transplantation (FMT) has shown potential for alleviating anxiety and depression, its effects remain understudied for individuals with AN. This study aims to determine whether oral capsular FMT is acceptable to adolescents with AN and results in clinical improvement in weight and/or psychological symptoms. METHODS: This study will randomise 20 adolescents with AN, ages 12-17 years, to receive either FMT or placebo capsules. These 20 youth, as well as an additional 10 youth who decline trial enrolment, will participate in qualitative interviews. We will track recruitment rates and collect psychological and biological measures (blood, stool, urine and saliva) at multiple timepoints to assess how gut microbiota and their metabolites may influence the symptoms of AN. Interviews with participants and caregivers will explore their experiences and views on FMT as a treatment approach. ETHICS AND DISSEMINATION: This study has received ethics approval by the Hamilton Integrated Research Ethics Board (#17493) and investigational drug approval by Health Canada (Dossier ID: c292423). Informed consent will be obtained by research staff from all participants. Findings will be disseminated through academic conferences, clinical forums and partnerships with advocacy organisations to reach clinicians, researchers and individuals with lived experience. TRIAL REGISTRATION NUMBER: NCT06593366.
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Degree of lipid saturation affects depressive-like behaviour and gut microbiota in mice.
This study explored the effects of the degree of lipid saturation on depressive behaviour and gut microbiota in mice. Thirty-two mice were divided into normal (N), Prozac (NP), lard (L) and fish oil (F) groups. After a 12-week dietary intervention, the open field test (OFT) and the forced swim test (FST) were conducted before sacrifice. The mice in the L group exhibited anxiety-like behaviours in the OFT and depressive-like behaviours in the FST. A significant difference was observed in β-diversity indices between the L group and the F group. The abundance of Allobaculum and Bifidobacterium was significantly higher in the F group than in the L and N groups. The prefrontal cortex fatty acid composition was altered in various lipid-treated groups and was highly correlated with depressive-like behaviours. In conclusion, the degree of lipid saturation affects depressive-like behaviour, gut microbiota composition, and the prefrontal cortex fatty acid profile in mice.
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Examining the relationship between the oral microbiome, alcohol intake and alcohol-comorbid neuropsychological disorders: protocol for a scoping review.
INTRODUCTION: Heavy alcohol use and alcohol use disorder (AUD) continues to rise as a public health problem and increases the risk for disease. Elevated rates of anxiety, depression, sleep disruption and stress are associated with alcohol use. Symptoms may progress to diagnosed neurophysiological conditions and increase risk for relapse if abstinence is attempted. Research on mechanisms connecting the gastrointestinal microbiome to neuropsychological disorders through the gut-brain axis is well-established. Less is known how the oral microbiome and oral microbial-associated biomarkers may signal to the brain. Therefore, a synthesis of research studying relationships between alcohol intake, alcohol-associated neurophysiological symptoms and the oral microbiome is needed to understand the state of the current science. In this paper, we outline our protocol to collect, evaluate and synthesise research focused on associations between alcohol intake and AUD-related neuropsychological disorders with the oral microbiome. METHODS AND ANALYSIS: The search strategy was developed and will be executed in collaboration with a medical research librarian. Studies will be screened by two independent investigators according to the aim of the scoping review, along with the outlined exclusion and inclusion criteria. After screening, data will be extracted and synthesised from the included papers according to predefined demographic, clinical and microbiome methodology metrics. ETHICS AND DISSEMINATION: A scoping review of primary sources is needed to synthesise the data on relationships between alcohol use, neuropsychological conditions associated with AUD and the oral microbiome. The proposed scoping review is based on the data from publicly available databases and does not require ethical approval. We expect the results of this synthesis will identify gaps in the growing literature and highlight potential mechanisms linking the oral-brain axis to addiction and other associated neuropsychological conditions. The study findings and results will be disseminated through journals and conferences related to psychology, neuroscience, dentistry and the microbiome.
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Pleiotropic modulation of the gut-brain-lung axis by ketamine and its enantiomers.
Ketamine, a potent N-methyl-D-aspartate receptor (NMDAR) antagonist, is widely used for anesthesia and analgesia and, because of its rapid antidepressant effects, in psychiatry. Increasing evidence suggests that ketamine and its enantiomers-(R)-ketamine (arketamine) and (S)-ketamine (esketamine)-also modulate systemic immunity and provide organ protection, partly through interactions with the gut microbiota, microbial metabolites, and intestinal immune-cell trafficking. However, these gut-mediated pathways must be distinguished from ketamine's well-established direct central and peripheral actions. In this review, we summarize how ketamine engages the gut-brain and gut-lung axes, emphasizing anti-inflammatory, immunoregulatory, and barrier-protective effects, while critically evaluating the evidence for causality in gut-organ communication. Along the gut-brain axis, ketamine is associated with restoration of microbial balance, normalization of short-chain fatty acid levels, and reduced migration of gut-derived γδ T17 and Th17 cells to the central nervous system, correlating with attenuated neuroinflammation and depressive-like behaviors. Through the gut-lung axis, ketamine has been reported to limit bacterial translocation and mesenteric lymph-associated inflammatory signaling and reduces pulmonary infiltration of pro-inflammatory cells, suggesting potential relevance in acute lung injury and other respiratory disorders. We also discuss enantiomer-specific effects: arketamine appears to provide more sustained neuroprotection and may be associated with fewer adverse effects than esketamine. Overall, these findings suggest the broad therapeutic potential of ketamine and its enantiomers for neuropsychiatric and inflammatory diseases, while underscoring the need for careful evaluation of long-term safety, optimal dosing, microbiota-targeted adjunctive strategies, and causal studies to distinguish direct pharmacological actions from indirect, microbiota-mediated effects.
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Host Microbiota Regulates Central Nervous System Serotonin Receptor 2C Editing in Rodents.
Microbial colonization of the gastrointestinal tract plays a crucial role in the development of enteric and central nervous system functionality. The serotonergic system has been heavily implicated in microbiota-gut-brain axis signaling, particularly in proof-of-principle studies in germ-free (GF) animals. One aspect of the serotonergic system that has been left unexplored in relation to the microbiota is the unique ability of the serotonin receptor 2C (5-HT2C) to undergo post-transcriptional editing, which has been implicated in decreased receptor functionality. We investigated whether GF mice, with absent microbiota from birth, have altered 5-HT2C receptor expression and editing in the brain, and if colonization of the microbiota is able to restore editing patterns. Next, we investigated whether microbiota depletion later in life using a chronic antibiotic treatment could affect 5-HT2C receptor editing patterns in rats. We found that GF mice have an increased prevalence of the edited 5-HT2C receptor isoforms in the amygdala, hypothalamus, prefrontal cortex, and striatum, which was partially normalized upon colonization post-weaning. However, no alterations were observed in the hypothalamus after microbiota depletion using an antibiotic treatment in adult rats. This suggests that alterations in the microbiome during development, but not later in life, could influence 5-HT2C receptor editing patterns. Overall, these results demonstrate that the microbiota affects 5-HT2C receptor editing in the brain and may inform novel therapeutic strategies in conditions in which 5-HT2C receptor editing is altered, such as depression.
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The Role of Gut Microbiota in Neuropsychiatric Diseases - Creation of An Atlas-Based on Quantified Evidence.
There is a growing body of evidence highlighting the significant role of gut microbiota in various pathologies. We performed a systematic review to review the different microbiota involved in neuropsychiatric diseases. 50 studies (23 studies for autism spectrum disorders, 18 for major depression, and 9 for schizophrenia), representing 2,137 patients and 2,844 controls. Concerning the microbiota, the genera Prevotella, Clostridium, Bacteroides, Bifidobacterium, Ruminococcus, Megamonas, and Faecalbacterium were the ones detected with the most frequent variation of their relatives abundance. We also assess the overlap between the different pathologies. This study provides new insights into the complex relationship between the brain and the gut and the implications in neuropsychiatric pathologies. The identification of unique signatures in neuropsychiatric diseases suggests new possibilities in targeted anti or probiotic treatment.
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Clinical and Immunologic Effects of Paraprobiotics in Long-COVID Patients: A Pilot Study.
BACKGROUND AND OBJECTIVES: After the enormous health burden during the acute stages of the COVID-19 pandemic, we are now facing another important challenge, that is, long-COVID, a clinical condition with often disabling signs and symptoms of the neuropsychiatric, gastrointestinal, respiratory, cardiovascular, and immune systems. While the pathogenesis of this syndrome is still poorly understood, alterations of immune function and the gut microbiota seem to play important roles. Because affected individuals are frequently unable to work for prolonged periods and suffer numerous health compromises, effective treatments represent a major unmet medical need. Multiple potential therapies have been tried, but none is approved yet. Approaches that are able to influence the immune system and gut microbiota such as probiotics and paraprobiotics, i.e., nonviable probiotics, seem promising candidates. We, therefore, evaluated the clinical and immunologic effects of paraprobiotics in a small pilot study. METHODS: A total of 6 patients with long-COVID were followed systematically for more than 12 months after disease onset using standardized validated questionnaires, a smartphone app, and wearable sensors to assess neurocognitive function, fatigue, depressiveness, autonomic nervous system alterations, and quality of life. We then offered patients defined paraprobiotics for 4 weeks and evaluated them at the end of the treatment period using the same questionnaires, smartphone app, and wearable sensors. In addition, a comprehensive immunophenotyping and gut microbiota analysis was performed before and after treatment. RESULTS: Improvements in several of the neurologic symptoms such as dysautonomia, fatigue, and depression were documented using both patient-reported outcomes and data from the smartphone app and wearable sensors. Of interest, the expression of activation markers on some immune cell populations such as B cells and nonclassical monocytes and the expression of toll-like receptor 2 (TLR2) on T cells were reduced after paraprobiotics treatment. DISCUSSION: Our results suggest that paraprobiotics might exert positive effects in patients with long-COVID most likely by modulating immune cell activation and expression of TLR2 on T cells. Further studies with paraprobiotics should confirm the promising observations of this small pilot study and hopefully not only improve the outcome of long-COVID but also unravel the pathomechanisms of this condition. CLASSIFICATION OF EVIDENCE: This study provides Class IV evidence that paraprobiotics increase the probability of favorable changes of clinical and immunologic markers in patients with long-COVID.