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The Gut Microbiome and Its Impact on Mood and Decision-Making: A Mechanistic and Therapeutic Review.
Background/Objectives: The gut microbiome is increasingly recognized as a key modulator of central nervous system function through the gut-brain axis. Dysbiosis has been associated with neuropsychiatric disorders such as depression, anxiety, impulsivity, cognitive decline, and addiction. This review aims to synthesize mechanistic insights and therapeutic perspectives on how gut microbiota influence mood regulation, decision-making, and cognitive processes. Methods: A comprehensive narrative review was conducted using peer-reviewed articles retrieved from PubMed, Scopus, and Web of Science up to August 2025. Studies were included if they explored microbiota-related effects on behavior, mood, cognition, or decision-making using human or animal models. Emphasis was placed on molecular mechanisms, microbiome-targeted therapies, and multi-omics approaches. Results: Evidence indicates that gut microbiota modulate neurochemical pathways involving serotonin, dopamine, GABA, and glutamate, as well as immune and endocrine axes. Microbial imbalance contributes to low-grade systemic inflammation, impaired neuroplasticity, and altered stress responses, all of which are linked to mood and cognitive disturbances. Specific microbial taxa, dietary patterns, and interventions such as probiotics, prebiotics, psychobiotics, and fecal microbiota transplantation (FMT) have shown promise in modulating these outcomes. The review highlights methodological advances including germ-free models, metagenomic profiling, and neuroimaging studies that clarify causal pathways. Conclusions: Gut microbiota play a foundational role in shaping emotional and cognitive functions through complex neuroimmune and neuroendocrine mechanisms. Microbiome-based interventions represent a promising frontier in neuropsychiatric care, although further translational research is needed to define optimal therapeutic strategies and address individual variability.
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Therapeutic modulation of the kynurenine pathway in severe mental illness and comorbidities: A potential role for serotonergic psychedelics.
Mounting evidence points towards a crucial role of the kynurenine pathway (KP) in the altered gut-brain axis (GBA) balance in severe mental illness (SMI, namely depression, bipolar disorder, and schizophrenia) and cardiometabolic comorbidities. Preliminary evidence shows that serotonergic psychedelics and their analogues may hold therapeutic potential in addressing the altered KP in the dysregulated GBA in SMI and comorbidities. In fact, aside from their effects on mood, psychedelics elicit therapeutic improvement in preclinical models of obesity, metabolic syndrome, and vascular inflammation, which are highly comorbid with SMI. Here, we review the literature on the therapeutic modulation of the KP in the dysregulated GBA in SMI and comorbidities, and the potential application of psychedelics to address the altered KP in the brain and systemic dysfunction underlying SMI and comorbidities. Psychedelics might therapeutically modulate the KP in the altered GBA in SMI and comorbidities either directly, via altering the metabolic pathway by influencing the rate-limiting enzymes of the KP and affecting the levels of available tryptophan, or indirectly, by affecting the gut microbiome, gut metabolome, metabolism, and the immune system. Despite promising preliminary evidence, the mechanisms and outcomes of the KP modulation with psychedelics in SMI and systemic comorbidities remain largely unknown and require further investigation. Several concerns are discussed surrounding the potential side effects of this approach in specific cohorts of individuals with SMI and systemic comorbidities.
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[The Therapeutic Potential of Prebiotics and Probiotics in Child and Adolescent Psychiatric Disorders].
The Therapeutic Potential of Prebiotics and Probiotics in Child and Adolescent Psychiatric Disorders Abstract: This short review summarizes the literature available on therapeutic interventions with prebiotics and probiotics and their potential use in psychiatric disorders in childhood, adolescence, and adulthood. Most studies of children and adolescents are done on ADHD and autism spectrum disorders, whereas single reports exist largely on positive effects on cognitive symptoms and quality of life. Initial studies regarding anorexia nervosa point to a potential effect of weight gain and reduction of gastrointestinal symptoms. To date, the effects of prebiotics and probiotics in depression, bipolar disorder, anxiety disorders, and schizophrenia have been mainly investigated in adults. The best reported evidence exists for depression, whereas the effects on depressive symptomatology are small. Positive effects are seen on gastrointestinal symptoms in these disorders. Given these positive effects, the mixed literature reports may result from very heterogeneous study designs. Nevertheless, the high potential of prebiotics and probiotics may be seen for minors with mental health problems. Further studies that include child and adolescent psychiatric populations and reflect the complexity of the gut-brain axis are urgently needed.
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Antibiotic use and the development of depression: A systematic review.
OBJECTIVE: Increasingly, disruption of the gastrointestinal ecosystem is thought to be involved in the pathogenesis of several medical conditions, including depression. Antibiotics can induce substantial changes in the gastrointestinal microbiota and several lines of evidence suggest that antibiotics exposure may increase the risk of developing depression. This systematic review examined this potential association. METHODS: PubMed, Ovid EMBASE, CINAHL, and PsychINFO databases, as well as unpublished resources, were searched for studies in humans published from 2000 onwards. The studies needed to consider the connection between antibiotic exposure (either alone or in combination with other antibiotics and medications) and the development of depressive symptoms and/or disorders (in isolation to other psychological conditions). RESULTS: Nine studies met the eligibility criteria. All were observational in nature. The studies were conducted in different age groups with various indications for receiving antibiotics. Together, these relatively low-quality studies suggest a potential association between antibiotic exposure and subsequent development of depression symptoms. Specifically, studies from the United Kingdom and Sweden indicate that the risk of depression is increased by at least 20%, with the former (over 1 million participants) reporting an increased risk with the number of courses and agents used, that persists with a slow decline over the ten years following exposure. CONCLUSIONS: The inherent limitations associated with the studies' methodologies make a reliable conclusion difficult. While the risk of antimicrobial resistance may prohibit large randomised clinical trials in healthy individuals, future placebo-controlled trials with antibiotics-based protocols (e.g. for acne) should explore their effect on mental health.
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Gut microbiome-derived ammonia modulates stress vulnerability in the host.
Ammonia has been long recognized as a metabolic waste product with well-known neurotoxic effects. However, little is known about the beneficial function of endogenous ammonia. Here, we show that gut ammonia links microbe nitrogen metabolism to host stress vulnerability by maintaining brain glutamine availability in male mice. Chronic stress decreases blood ammonia levels by altering gut urease-positive microbiota. A representative urease-producing strain, Streptococcus thermophilus, can reverse depression-like behaviours induced by gut microbiota that was altered by stress, whereas pharmacological inhibition of gut ammonia production increases stress vulnerability. Notably, abnormally low blood ammonia levels limit the brain's availability of glutamine, a key metabolite produced by astrocytes that is required for presynaptic γ-aminobutyric acid (GABA) replenishment and confers stress vulnerability through cortical GABAergic dysfunction. Of therapeutic interest, ammonium chloride (NH4Cl), a commonly used expectorant in the clinic, can rescue behavioural abnormalities and GABAergic deficits in mouse models of depression. In sum, ammonia produced by the gut microbiome can help buffer stress in the host, providing a gut-brain signalling basis for emotional behaviour.
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Mitochondria and immunity in chronic fatigue syndrome.
It is widely accepted that the pathophysiology and treatment of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) could be considerably improved. The heterogeneity of ME/CFS and the confusion over its classification have undoubtedly contributed to this, although this would seem a consequence of the complexity of the array of ME/CFS presentations and high levels of diverse comorbidities. This article reviews the biological underpinnings of ME/CFS presentations, including the interacting roles of the gut microbiome/permeability, endogenous opioidergic system, immune cell mitochondria, autonomic nervous system, microRNA-155, viral infection/re-awakening and leptin as well as melatonin and the circadian rhythm. This details not only relevant pathophysiological processes and treatment options, but also highlights future research directions. Due to the complexity of interacting systems in ME/CFS pathophysiology, clarification as to its biological underpinnings is likely to considerably contribute to the understanding and treatment of other complex and poorly managed conditions, including fibromyalgia, depression, migraine, and dementia. The gut and immune cell mitochondria are proposed to be two important hubs that interact with the circadian rhythm in driving ME/CFS pathophysiology.
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The endocannabinoidome-gut microbiome-brain axis as a novel therapeutic target for autism spectrum disorder.
INTRODUCTION: Autism spectrum disorder (ASD) is characterized by disruption of the gut-brain axis, which leads to behavioral, psychiatric, metabolic and gastrointestinal symptoms. Effective ASD treatments are limited. Research highlights the roles of the endocannabinoidome (eCBome) and gut microbiome (GM), both crucial for brain and gut function. This review summarizes research on therapeutic targets within the eCBome-GM-brain axis for ASD and related comorbidities. DISCUSSION: Evidence suggests that reduced levels of eCBome mediators, like oleoylethanolamide and anandamide, and altered cannabinoid type 1 and type 2 (CB1 and CB2) receptors activity may contribute to ASD symptoms, making them promising targets. Modulating the eCBome-GM-brain axis with inhibitors of fatty acid amide hydrolase (FAAH), transient receptor potential vanilloid 1, and monoacylglycerol lipase (MAGL) may improve repetitive, stereotypical, and sensory behaviors, and alleviate sociability impairments, depression and anxiety. However, inhibition of FAAH and MAGL may also induce ADHD-like behaviors, which can be reversed by CB1 inverse agonists. Targeting metabotropic glutamate receptor 5 to increase levels of the eCBome mediator 2-arachidonoylglycerol (2-AG) may benefit ASD-related behaviors. eCBome mediators such as 2-AG, 1/2-palmitoylglycerol and palmitoylethanolamide may also help manage ASD- and GI-related symptoms, and systemic inflammation. Other potential therapeutic targets that deserve further investigation are eCBome-related receptors G-protein-coupled receptor 55 and peroxisome proliferator-activated receptors-alpha and -gamma, and the cyclooxygenase-2/prostaglandin E2 pathway, which may address hyperactivity and repetitive behaviors. Additionally, mucin-degrading genera like Akkermansia and Ruminococcus may improve ASD-related GI symptoms such as hypersensitivity and inflammation. Selective antibiotics against specific Clostridium strains may improve irritability and aggression. In ASD with ADHD and OCD, treatments may involve modulating the CB1 and CB2 receptor, and bacterial families like Ruminococcaceae and Lachnospiraceae. Lastly, modulating the abundance of anti-inflammatory genera like Prevotella and Anaeroplasma, and taxa associated with gut health such as Roseburia may also offer therapeutic value. CONCLUSION: The eCBome-GM-brain axis is a promising target for ASD treatment, meriting further clinical and preclinical research.
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Gut microbiota-derived extracellular vesicles: Exploring the pathogenesis and treatment of neuropsychiatric disorders.
The gut microbiome is connected to the pathogenesis of various neuropsychiatric disorders, including cognitive impairment and depression. The gut microbiota can act on the brain through multiple pathways along the gut-brain axis. However, the specific mechanisms are unclear. Bacterial extracellular vesicles (BEVs), bacteria-derived membrane-bound vesicles that can carry a variety of bioactive substances and cross various barriers in the host, are used by bacteria to communicate and interact with the host. Recent studies have shown that BEVs from the gut microbiota are involved in gut-brain communication and may play a role in the pathogenesis and treatment of neuropsychiatric disorders. This review provides an overview of the biogenesis, structure, and function of BEVs and emphasizes their role in the development and treatment of neuropsychiatric disorders.
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Gut microbiota dysbiosis at the interface of neuropsychiatric disorders and their dermatological comorbidities.
Neuropsychiatric disorders such as autism spectrum disorder (ASD), generalized anxiety disorder (GAD), major depressive disorder (MDD), and schizophrenia (SZ) frequently co-occur with dermatological conditions, including atopic dermatitis, psoriasis, rosacea, and chronic urticaria. The biologic basis remains incompletely understood. A growing body of evidence implicates gut microbiota dysbiosis as a shared pathogenic factor linking these conditions. This review synthesizes preclinical and clinical findings demonstrating consistent microbial alterations across both neuropsychiatric and dermatologic conditions, including fluctuations in alpha diversity, disrupted Firmicutes/Bacteroidetes ratios, and depletion of short-chain fatty acid (SCFA)-producing taxa such as Faecalibacterium, Roseburia, and Eubacterium species. These microbial shifts parallel elevations in inflammatory mediators such as interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β), and interleukin-17 (IL-17), and cause perturbations in amino acid metabolism, altered glutamate-GABA signaling and increased branched-chain amino acids, indicating convergence on immune and metabolic pathways. Experimental rodent studies support the concept by demonstrating that microbiota dysbiosis can both impact psychiatric-like behaviors and cutaneous inflammation. Microbiota-targeted therapies such as probiotics show preliminary efficacy in improving symptoms across both domains. These findings support a gut microbiota-brain-skin axis and suggest that targeting gut dysbiosis may offer an integrated therapeutic approach for neuropsychiatric disorders and their dermatologic comorbidities.
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Disruption of the gut microbiota-inflammation-brain axis in unmedicated bipolar disorder II depression.
The relationships of the gut microbiota-inflammation-brain axis in depressive bipolar disorder (BD) remains under-elaborated. Sixty-five unmedicated depressive patients with BD II and 58 controls (HCs) were prospectively enrolled. Resting-state functional MRI data of static and dynamic amplitude of low-frequency fluctuation (ALFF) was measured, and abnormal ALFF masks were subsequently set as regions of interest to calculate whole-brain static functional connectivity (sFC) and dynamic functional connectivity (dFC). Fecal samples were collected to assess gut diversity and enterotypes using 16S amplicon sequencing. Blood samples were also collected, serum was assayed for levels of cytokines (interleukin [IL]-2, IL-4, IL-6, IL-8, IL-10, tumor necrosis factor [TNF]-α). Patients with BD II exhibited decreased static ALFF values in the left cerebellum Crus II, and decreased cerebellar sFC and dFC to the right inferior parietal lobule and right superior frontal gyrus, respectively. Moreover, higher pro-inflammatory and anti-inflammatory cytokines levels, and increased proinflammatory bacteria and glutamate and gamma-aminobutyric acid metabolism related bacteria were identified in BD II. The interaction of Parabacteroides levels × IL-8 levels was an independent contributor to static ALFF in the left cerebellar Crus II. The findings bridged a gap in the underlying pathophysiological mechanism of the gut microbiota-inflammation-brain axis in BD II depression.