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Gut Microbiota Modulation in CNS Disorders: Therapeutic Strategies and Implications for Drug Efficacy.
Various central nervous system (CNS) disorders, including neurodegenerative diseases, depression, schizophrenia, epilepsy, and anxiety, present significant obstacles to public health because of their intricate causes and the scarcity of effective treatments. Recent studies have shown that gut microbiota (GM) and CNS communicate bidirectionally. Modulation of immune system, neurotransmitters, and neuroactive metabolites are only a few examples of how GM can significantly influence CNS. Dysbiosis or changes in composition and function of gut microbes play a contributing role in various CNS disorders. In these disorders, probiotics, prebiotics, fecal microbiota transplantation, antibiotics use, and interventions based on microbial metabolites have demonstrated beneficial effects in animal models and some clinical studies. By restoring microbial equilibrium, increasing microbial diversity, and promoting the generation of beneficial metabolites, these approaches can improve the efficacy of traditional medications while minimizing their side effects and the disease itself, based on preclinical evidence and emerging clinical studies. Nevertheless, several obstacles should be overcome before the clinical translation of these approaches, such as using of standardized methods for modulating GM, identifying specific microbial signatures linked to various CNS illnesses, and understanding the exact mechanisms of gut-brain communication. This review provides a novel integrated perspective by comprehensively clarifying the bidirectional interactions between CNS pharmacological agents and microbiota-based therapeutic strategies in different neurological and psychiatric disorders, offering a unified framework to improve traditional pharmacological therapies. Importantly, future studies should concentrate on exploring the mechanisms and the exact interconnections between GM and CNS problems to elaborate targeted therapies for these disorders.
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Biosignals in the Gut-Brain Axis Transmission: Function and Detection.
The gut-brain axis (GBA) is an important information pathway connecting the brain, the central nervous system (CNS), and the gastrointestinal (GI) tract. On the one hand, gut microbiota can influence the function brain through GBA; on the other hand, the brain can also change the structural composition of gut microbiota via GBA. It contains a myriad of biosignals, such as monoamines, inflammatory cytokines, and macro-biomolecules, as the information carriers. Highly selective, sensitive, and reliable sensing techniques are essential to resolve the specific function of individual biosignals. This review summarizes the widely reported biosignals related to GBA and their functions, and organizes the latest sensing tools to provide feasible characterization ideas for GBA-related work. In addition, these low-cost, fast-responding sensors can also be used for early identification and diagnosis of GBA-related diseases (e.g., depression). Finally, the problems and deficiencies in this field are pointed out to provide a reference for the orientation of researchers in the sensing field.
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Gut microbiota alterations in stable outpatients with schizophrenia: findings from a case-control study.
OBJECTIVE: The pathogenesis of schizophrenia is multidimensional and intensively studied. The gut-brain axis disturbances might play a significant role in the development of schizophrenia. METHODS: We compared the gut microbiota of 53 individuals with schizophrenia and 58 healthy controls, using the 16S rRNA sequencing method. Individuals with schizophrenia were assessed using the following scales: the Positive and Negative Syndrome Scale, the Calgary Depression Scale for Schizophrenia, the Social and Occupational Functioning Assessment Scale and the Repeatable Battery for the Assessment of Neuropsychological Status. RESULTS: No significant between-group differences in α-diversity measures were observed. Increased abundance of Lactobacillales (order level), Bacilli (class level) and Actinobacteriota (phylum level) were found in individuals with schizophrenia regardless of potential confounding factors, and using two independent analytical approaches (the distance-based redundancy analysis and the generalised linear model analysis). Additionally, significant correlations between various bacterial taxa (the Bacteroidia class, the Actinobacteriota phylum, the Bacteroidota phylum, the Coriobacteriales order and the Coriobacteria class) and clinical manifestation (the severity of negative symptoms, performance of language abilities, social and occupational functioning) were observed. CONCLUSIONS: The present study indicates that gut microbiota alterations are present in European patients with schizophrenia. The abundance of certain bacterial taxa might be associated with the severity of negative symptoms, cognitive performance and general functioning. Nonetheless, additional studies are needed before the translation of our results into clinical practice.
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Finding the needle in the haystack: systematic identification of psychobiotics.
The brain-gut-microbiota axis is increasingly viewed as a novel paradigm in neuroscience with the capacity to generate innovative therapies for patients with psychiatric illnesses. Psychobiotics, defined as live bacteria, which when ingested in adequate amounts, confer mental health benefits, are increasingly of interest, as preclinical trials continue to show promising results. Particularly in stress-related, anxiety and depressive disorders, there is potential for psychobiotics to deliver new therapies. The question of which microbes may prove to be the most promising psychobiotic in delivering such therapies at a clinical level is of great importance. Here we look at the characteristics of psychobiotics, in an attempt to present an outline from which the identification of potential new psychobiotics may be possible. LINKED ARTICLES: This article is part of a themed section on When Pharmacology Meets the Microbiome: New Targets for Therapeutics? To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v175.24/issuetoc.
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Lacidophilin tablets relieve irritable bowel syndrome in rats by regulating gut microbiota dysbiosis and intestinal inflammation.
Irritable bowel syndrome (IBS) is a common clinical functional gastrointestinal disease. It has a complex pathophysiological mechanism, in which the imbalance of gut microbiota might play an important role. Lacidophilin tablets (LH) can regulate gut microbiota, but their effect on IBS is unknown. In this study, the IBS model was established by acetic acid enema combined with the constrained stress method, and rats were fed LH for 2 weeks. LH significantly reduced visceral sensitivity and intestinal propulsion rate and improved IBS-induced anxiety and depressive behavior in IBS rats. LH elevated the expression levels of mucin 2, claudin1, and occludin, and ameliorated IBS-induced structural damage to colonic tissues. The gut microbiota analysis revealed that LH altered the structure and composition of the gut microbiota in IBS rats. In addition, LH reduced the expression levels of inflammatory factor-related genes. These results suggest that LH could significantly improve the visceral sensitivity and intestinal motility disorders of IBS rats, relieve anxiety and depression levels, and alleviate the symptoms of IBS rats by regulating gut microbiota and reducing intestinal inflammation.
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The gut microbiota is associated with psychiatric symptom severity and treatment outcome among individuals with serious mental illness.
BACKGROUND: Emerging evidence implicates the gut microbiota in central nervous system functioning via its effects on inflammation, the hypothalamic-pituitary axis, and/or neurotransmission. Our understanding of the cellular underpinnings of the brain-gut relationship is based almost exclusively on animal models with some small-scale human studies. This study examined the relationship between the gut microbiota and psychiatric symptom severity and treatment response among inpatients with serious mental illness. METHOD: We collected data from adult inpatients (N = 111). Measures of diagnoses, suicide severity, trauma, depression, and anxiety were collected shortly after admission, while self-collected fecal swabs were collected early in the course of hospitalization and processed using 16S rRNA gene sequencing and whole genome shotgun sequencing methods. RESULTS: Results indicate that depression and anxiety severity shortly after admission were negatively associated with bacterial richness and alpha diversity. Additional analyses revealed a number of bacterial taxa associated with depression and anxiety severity. Gut microbiota richness and alpha diversity early in the course of hospitalization was a significant predictor of depression remission at discharge. CONCLUSIONS: This study is among the first to demonstrate a gut microbiota relationship with symptom severity among psychiatric inpatients as well as a relationship to remission of depression post-treatment. These findings are consistent with animal models and limited human studies as well as with the broader literature implicating inflammation in the pathophysiology of depression. These findings offer the foundation for further studies of novel therapeutic approaches to the treatment, prevention of, or recurrence of serious mental illness.
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Experiencing social exclusion changes gut microbiota composition.
Gut microbiota is suggested to regulate the host's mental health via the gut-brain axis. In this study, we investigated the relationship between the microbiome and psychological pain due to social exclusion. Adult individuals with (n = 14) and without (n = 25) social exclusion experience were assessed for the psychological status using self-reported questionnaires: Beck Anxiety Inventory (BAI), Beck Depression Inventory, and the UCLA Loneliness Scale. The gut microbiota was analyzed by 16 S rRNA gene sequencing and bioinformatics. The exclusion group had a 1.70-fold higher total BAI score and 2.16-fold higher levels of anxiety-related physical symptoms (p < 0.05). The gut microbial profiles also differed between the two groups. The exclusion group showed higher probability of having Prevotella-enriched microbiome (odds ratio, 2.29; 95% confidence interval, 1.65-2.75; p < 0.05), a significantly reduced Firmicutes/Bacteroidetes ratio, and decreased abundance of Faecalibacterium spp. (p < 0.05) which was associated with the duration and intensity of social exclusion (p < 0.05). Our results indicate that the psychological pain due to social exclusion is correlated with the gut microbiota composition, suggesting that targeting social exclusion-related microorganisms can be a new approach to solving psychological problems and related social issues.
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The microbiota-gut-brain axis in neuropsychiatric disorders: Mechanisms, advances, and clinical applications.
Neuropsychiatric disorders are increasingly recognized as systemic conditions arising from dynamic interactions within the gut-brain-immune network. The Microbiota-Gut-Brain Axis (MGBA) serves as a central regulatory system orchestrating neurodevelopment, neural homeostasis, and immune-metabolic balance. This review summarizes evidence across seven major neuropsychiatric disorders, Depression, Autism Spectrum Disorder, Attention-Deficit/Hyperactivity Disorder, Alzheimer's disease, Schizophrenia, Anxiety and Obsessive Compulsive Disorder, demonstrating that dysregulation of the MGBA constitutes a shared pathological mechanism. On this common basis, we delineate disorder specific neurochemical and immunological features and highlight the clinical potential of microbiota-targeted interventions. Moreover, psychotropic medications profoundly alter microbial physiology, influencing bacterial growth and metabolism, thereby complicating interpretation of MGBA-disease relationships. Future research should define strain-specific therapeutic actions and integrate multi-omics approaches to unravel causal pathways, ultimately enabling precision microbiome modulation in neuropsychiatric medicine.
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Exploiting the gut microbiota's fermentation capabilities towards disease prevention.
One of the crucial roles played in the context of human physiology by the human gut microbiota is to ferment resistant polysaccharides and dietary fibres in the colon. Even though it has long been presumed that these processes play fundamental roles in regulating human health, we remain unable to treat or even diagnose deficiencies in microbial fermentation. In part, this relatively slow progress can be attributed to the fact that studying the gut microbiota and its metabolic properties has until now heavily relied on next generation sequencing and case-control cohorts to identify differentially abundant genes, pathways or organisms in the context of a particular clinical indication. Unfortunately, these methods and studies do not allow us to rigorously probe the functional and metabolic phenotype of a microbiota, or for elucidating its mechanisms of action on the host. To improve our clinical control over these fermentation processes, it is critical that we improve our quantitative, mechanistic understanding of their impact on host physiology. In this review, we provide an overview of our current understanding of the roles microbial fermentation processes play in human health in the context of disease prevention. We then describe the evidence linking these processes with depression and anxiety-related conditions, and use these complex disorders as a framework for illustrating the fact that achieving a clinical vision that exploits microbial fermentation towards human health will depend on thoughtful multi-disciplinary collaboration between clinical research, systems biology, and the pharmaceutical and analytical sciences.
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Microbial alpha diversity in the intestine negatively correlated with disease duration in patients with Meniere's disease.
Ménière's disease (MD) is characterized by loss of balance and hearing disorders. Although there is known to be endolymphatic hydrops involved in the pathological process, the pathogenesis of the disease is still largely unclear. Approximately half of patients with MD suffer from depressive symptoms and high levels of several stress hormones were observed in MD and depression, simultaneously. Recently, gut microbes have been shown to influence the function of the central nervous system in humans through their metabolites. We studied the intestinal microbiota of 10 patients with MD and 11 healthy donors (HD). Significant negative correlations were found between disease duration and alpha diversity indexes of gut microbes in patients with MD. The relative abundance of the species Butyricicoccus ambiguous taxa was increased in patients with MD compared with that of HD. In contrast, Oscillospiraceae UCG-002/UCG-005 ambiguous taxa and Anaerovoracaceae (Eubacterium) brachy group uncultured bacterium were increased in the relative abundance of HD than that of patients with MD. The relative abundance of the Butyricicoccus species was positively correlated with disease duration. Thus, these compositional alterations of gut microbes in patients with MD are associated with inner ear pathologies, such as endolymphatic hydrops, by changing the metabolite profiles in the intestine.