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The contribution of gut-brain axis to development of neurological symptoms in COVID-19 recovered patients: A hypothesis and review of literature.
The gut microbiota undergoes significant alterations in response to viral infections, particularly the novel SARS-CoV-2. As impaired gut microbiota can trigger numerous neurological disorders, we suggest that the long-term neurological symptoms of COVID-19 may be related to intestinal microbiota disorders in these patients. Thus, we have gathered available information on how the virus can affect the microbiota of gastrointestinal systems, both in the acute and the recovery phase of the disease, and described several mechanisms through which this gut dysbiosis can lead to long-term neurological disorders, such as Guillain-Barre syndrome, chronic fatigue, psychiatric disorders such as depression and anxiety, and even neurodegenerative diseases such as Alzheimer's and Parkinson's disease. These mechanisms may be mediated by inflammatory cytokines, as well as certain chemicals such as gastrointestinal hormones (e.g., CCK), neurotransmitters (e.g., 5-HT), etc. (e.g., short-chain fatty acids), and the autonomic nervous system. In addition to the direct influences of the virus, repurposed medications used for COVID-19 patients can also play a role in gut dysbiosis. In conclusion, although there are many dark spots in our current knowledge of the mechanism of COVID-19-related gut-brain axis disturbance, based on available evidence, we can hypothesize that these two phenomena are more than just a coincidence and highly recommend large-scale epidemiologic studies in the future.
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Neuroplasticity and the microbiome: how microorganisms influence brain change.
Neuroplasticity, the brain's ability to reorganize and adapt, has traditionally been attributed to external stimuli, learning, and experience. However, emerging research highlights the gut microbiota as a key modulator of neuroplasticity through the gut-brain axis. This review examines the mechanisms by which intestinal microorganisms influence brain function, including microbial metabolite production, immune system modulation, neurotransmitter synthesis, and hormonal regulation. Dysbiosis, or microbial imbalance, has been linked to neurodevelopmental disorders, major depressive disorder (MDD), and cognitive impairments, emphasizing the microbiome's role in psychiatric and neurological health. Animal and human studies suggest that microbiota-targeted interventions, such as probiotics, prebiotics, and dietary modifications, may enhance neuroplasticity and mitigate mental health disorders. Future research should focus on understanding direct microbial-neuronal interactions and developing personalized microbiome-based therapies. This study underscores the gut microbiota's potential as a novel target for improving brain plasticity and mental health outcomes.
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Gut Regulated Associations of Neuronal Signalling in High Blood Pressure (GRAINS-BP): a double-blinded randomised crossover placebo-controlled trial.
BACKGROUND: Hypertension affects 1 in 3 Australian adults and is a major contributor to stroke and myocardial infarction. Despite the availability of various medications, over 50% of patients struggle to control their blood pressure (BP) due to nonadherence, difficulty finding the right treatment, or avoidance of medication. Diet plays a key role in cardiovascular health, with high-fiber intake shown to lower BP through the production of short-chain fatty acids (SCFAs), metabolites formed during fiber fermentation. A previous clinical trial found that incorporating a specific type of resistant starch - high amylose maize starch enriched with acetate and butyrate (HAMSA/B) - significantly reduced blood pressure in hypertensive patients. While the exact mechanism remains unclear, SCFAs may influence BP via the gut-brain axis by reducing muscle sympathetic nerve activity (MSNA), which has vasoconstrictor function and is elevated in hypertensive individuals. METHODS: The GRAINS-BP clinical trial will recruit 29 adults with untreated hypertension (≥ 140/90 mmHg) for a double-blind, cross-over study using HAMSA/B administered as a shake delivered twice daily. The assessment period will span 48 days and include four visits at the Alfred Hospital, Melbourne, Australia. At visit 1, baseline measurement will be taken, including muscle sympathetic nerve activity (MSNA) and electrocardiogram (ECG). Participants will be randomised to the order in which they receive the placebo and HAMSA/B shake. Each intervention period will last 14 days, separated by a 20-day washout before participants cross over to the alternate treatment. At each visit, faecal, urine, and blood samples will be collected to investigate microbiome, cardiometabolic, renal, and immune profiles, respectively. Univariate and multivariate statistical analyses will be conducted to examine treatment effects and to identify correlations among microbiome, cardiometabolic, renal, and immune outcomes. DISCUSSION: This project's primary outcome is change in autonomic nervous system activity. Secondary outcomes include 24-h BP, gut microbiome composition, SCFA levels, immune cell profiles gastrointestinal transit time, quality of life, anxiety and depression symptoms, cognitive function, gut barrier integrity, and circulating micro- and nanoplastics. Findings from this study will reveal whether SCFAs reduce blood pressure by their influence on the autonomic nervous system. TRIAL REGISTRATION: This trial is registered with the Australian New Zealand Clinical Trials Registry (ACTRN12625000557437).
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Therapeutic Anti-Depressant Potential of Microbial GABA Produced by Lactobacillus rhamnosus Strains for GABAergic Signaling Restoration and Inhibition of Addiction-Induced HPA Axis Hyperactivity.
The role of the microbiota-gut-brain (MGB) axis in mood regulation and depression treatment has gained attention in recent years, as evidenced by the growing number of animal and human studies that have reported the anti-depressive and associated gamma-aminobutyric acid-ergic (GABAergic) effects of probiotics developed from Lactobacillus rhamnosus bacterial strains in the gut microbiome. The depressive states attenuated by these probiotics in patients suffering from clinical depression also characterize the severe and relapse-inducing withdrawal phase of the addiction cycle, which has been found to arise from the intoxication-enabled hyperregulation of the hypothalamic-pituitary-adrenal (HPA) axis, the body's major stress response system, and a corresponding attenuation of its main inhibitory system, the gamma-aminobutyric acid (GABA) signaling system. Therefore, the use of probiotics in the treatment of general cases of depression provides hope for a novel therapeutic approach to withdrawal depression remediation. This review discusses potential therapeutic avenues by which probiotic application of Lactobacillus rhamnosus strains can be used to restore the central GABAergic activity responsible for attenuating the depression-inducing HPA axis hyperactivity in addiction withdrawal. Also, information is provided on brain GABAergic signaling from other known GABA-producing strains of gut microbiota.
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Serotonin Transporter Genotype Modulates the Gut Microbiota Composition in Young Rats, an Effect Augmented by Early Life Stress.
The neurotransmitter serotonin (5-HT) plays a vital regulatory role in both the brain and gut. 5-HT is crucial for regulating mood in the brain as well as gastrointestinal motility and secretion peripherally. Alterations in 5-HT transmission have been linked to pathological symptoms in both intestinal and psychiatric disorders and selective 5-HT transporter (5-HTT) inhibitors, affecting the 5-HT system by blocking the 5-HT transporter (5-HTT) have been successfully used to treat CNS- and intestinal disorders. Humans that carry the short allele of the 5-HTT-linked polymorphic region (5-HTTLPR) are more vulnerable to adverse environmental stressors, in particular early life stress. Although, early life stress has been shown to alter the composition of the gut microbiota, it is not known whether a lower 5-HTT expression is also associated with an altered microbiome composition. To investigate this, male and female wild type (5-HTT+/+), heterozygous (5-HTT+/-), and knockout (5-HTT-/-) 5-HT transporter rats were maternally separated for 6 h a day from postnatal day 2 till 15. On postnatal day 21, fecal samples were collected and the impact of 5-HTT genotype and maternal separation (MS) on the microbiome was analyzed using high-throughput sequencing of the bacterial 16S rRNA gene. MS showed a shift in the ratio between the two main bacterial phyla characterized by a decrease in Bacteroidetes and an increase in Firmicutes. Interestingly, the 5-HTT genotype caused a greater microbal dysbiosis (microbial imbalance) compared with MS. A significant difference in microbiota composition was found segregating 5-HTT-/- apart from 5-HTT+/- and 5-HTT+/+ rats. Moreover, exposure of rats with 5-HTT diminished expression to MS swayed the balance of their microbiota away from homeostasis to 'inflammatory' type microbiota characterized by higher abundance of members of the gut microbiome including Desulfovibrio, Mucispirillum, and Fusobacterium, all of which are previously reported to be associated with a state of intestinal inflammation, including inflammation associated with MS and brain disorders like multiple depressive disorders. Overall, our data show for the first time that altered expression of 5-HTT induces disruptions in male and female rat gut microbes and these 5-HTT genotype-related disruptions are augmented when combined with early life stress.
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Cognitive Function and the Microbiome.
There is increasing evidence that the composition of the resident bacteria within the gastrointestinal tract can influence the brain and behavior, particularly with respect to cognitive function. Cognitive function encompasses the life-long process of learning, both long- and short-term processes. Cognition was originally thought to be exclusively regulated by the central nervous system, with long-term potentiation and neurogenesis contributing to the creation and storage of memories, but now other systems, including, for example, the immune system and the intestinal microbiome may also be involved. Cognitive impairment has been identified in numerous disease states, both gastrointestinal and extraintestinal in nature, many of which have also been characterized as having a role for dysbiosis in disease pathogenesis. This includes, but is not limited to, inflammatory bowel diseases, irritable bowel syndrome, type 1 diabetes, obesity, major depressive disorder, and autism spectrum disorder. The role of cognition and the microbiome will be discussed in this chapter for all these diseases, as well as evidence for a role in maintaining overall human health and well being. Finally, evidence for a role for probiotics in beneficially modulating the microbiota and leading to improved cognition will be discussed.
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Early life adversity predicts brain-gut alterations associated with increased stress and mood.
Alterations in the brain-gut system have been implicated in various disease states, but little is known about how early-life adversity (ELA) impacts development and adult health as mediated by brain-gut interactions. We hypothesize that ELA disrupts components of the brain-gut system, thereby increasing susceptibility to disordered mood. In a sample of 128 healthy adult participants, a history of ELA and current stress, depression, and anxiety were assessed using validated questionnaires. Fecal metabolites were measured using liquid chromatography tandem mass spectrometry-based untargeted metabolomic profiling. Functional brain connectivity was evaluated by magnetic resonance imaging. Sparse partial least squares-discriminant analysis, controlling for sex, body mass index, age, and diet was used to predict brain-gut alterations as a function of ELA. ELA was correlated with four gut-regulated metabolites within the glutamate pathway (5-oxoproline, malate, urate, and glutamate gamma methyl ester) and alterations in functional brain connectivity within primarily sensorimotor, salience, and central executive networks. Integrated analyses revealed significant associations between these metabolites, functional brain connectivity, and scores for perceived stress, anxiety, and depression. This study reveals a novel association between a history of ELA, alterations in the brain-gut axis, and increased vulnerability to negative mood and stress. Results from the study raise the hypothesis that select gut-regulated metabolites may contribute to the adverse effects of critical period stress on neural development via pathways related to glutamatergic excitotoxicity and oxidative stress.
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From gums to moods: Exploring the impact of the oral microbiota on depression.
Depression is a complex and heterogeneous disorder that results from a combination of genetic vulnerability, environmental stressors, and dysregulated biological processes. While systemic inflammation and gut dysbiosis have been extensively investigated in the context of depression, the role of the oral microbiome has only recently begun to emerge. The oral microbiome is a highly diverse and dynamic ecosystem, comprising bacteria, fungi, viruses, and archaea, which coexist in a delicate balance with the host's immune system. This microbial community plays a fundamental role in maintaining not only oral health, but also systemic homeostasis. Emerging evidence suggests that disruptions in this balance, or oral dysbiosis, may contribute to a range of systemic inflammatory conditions, including psychiatric disorders such as depression. Factors comprising periodontal disease, dental infections, and poor oral hygiene can lead to an imbalance in oral microbial composition, promoting immune system activation, chronic inflammation and microbial translocation, which are increasingly recognised mechanisms involved in the pathophysiology of depression. This review delves into the emerging evidence linking oral dysbiosis to depression, elucidating the underlying biological mechanisms and their clinical implications. By bridging the gap between oral health and mental well-being, it underscores the importance of a multidisciplinary approach in addressing depression-one that extends beyond conventional psychiatric treatments to include oral health interventions as a viable component of comprehensive care strategies.
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Role of PPAR-Allopregnanolone Signaling in Behavioral and Inflammatory Gut-Brain Axis Communications.
The gut microbiome regulates emotional behavior, stress responses, and inflammatory processes by communicating with the brain. How and which neurobiological mediators underlie this communication remain poorly understood. PPAR-α (peroxisome proliferator-activated receptor α), a transcription factor susceptible to epigenetic modifications, regulates pathophysiological functions, including metabolic syndrome, inflammation, and behavior. Mood disorders, inflammatory processes, and obesity are intertwined phenomena that are associated with low blood concentrations of the anti-inflammatory and "endogenous tranquilizer" neurosteroid allopregnanolone and poor PPAR-α function. Stress and consumption of obesogenic diets repress PPAR function in brain, enterocytes, lipocytes, and immune modulatory cells favoring inflammation, lipogenesis, and mood instability. Conversely, micronutrients and modulators of PPAR-α function improve microbiome composition, dampen systemic inflammation and lipogenesis, and improve anxiety and depression. In rodent stress models of anxiety and depression, PPAR activation normalizes both PPAR-α expression downregulation and decreased allopregnanolone content and ameliorates depressive-like behavior and fear responses. PPAR-α is known to regulate metabolic and inflammatory processes activated by short-chain fatty acids; endocannabinoids and congeners, such as N-palmitoylethanolamide, drugs that treat dyslipidemias; and micronutrients, including polyunsaturated fatty acids. Both PPAR-α and allopregnanolone are abundantly expressed in the colon, and they exert potent anti-inflammatory actions by blocking the toll-like receptor-4-nuclear factor-κB pathway in peripheral immune cells, neurons, and glia. The perspective that PPAR-α regulation in the colon by gut microbiota or metabolites influences central allopregnanolone content after trafficking to the brain, thereby serving as a mediator of gut-brain axis communications, is examined in this review.
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Mind gut harmony: psychobiotics effects on the gut-brain axis and harnessing its effects for the mental health.
The microbiota-gut-brain axis is gaining attention as a potential therapeutic avenue for treating illnesses of the illnesses of the central nervous system. In recent years, there has been a notable increase in literature examining the connection between the gut microbiome and its impact on overall health and wellness. The microbiota-gut-brain axis is a promising therapeutic target for treating central nervous system diseases and reducing drug adverse effects. Probiotics have been shown in pre-clinical and clinical trials to improve health by modulating the microbiota in the gut-brain axis. Psychobiotics are probiotics that modulate the gut-brain axis (GBA) and regulate the central nervous system to improve gastrointestinal function, as well as have antidepressant and anxiolytic properties via neuronal, humoral, and metabolic mechanisms. Some psychobiotic strains have been shown to reduce inflammation and cortisol levels, thereby degenerative and neurodevelopmental illnesses such as Parkinson's disease, Alzheimer's disease, and autism spectrum disorder can be effectively treated with psychobiotics. Alleviating anxiety and depression symptoms. Neurodegenerative and neurodevelopmental illnesses such as Parkinson's disease, Alzheimer's disease, and autism spectrum disorder can be effectively treated with psychobiotics. This review summarizes the psychobiotic potential on the gut-brain axis for the mental health.