Search Results (1,164)

Background/Objectives: Growing evidence suggests that the gut–brain axis influences brain function, particularly the role of intestinal microbiota in modulating cognitive processes. Probiotics may alter brain function and behavior by modulating gut microbiota, with implications for neurodegenerative diseases like Alzheimer’s disease (AD). The purpose of this review is to systematically review the current literature exploring the effects of probiotic supplementation on gut microbiota and cognitive function in AD and mild cognitive impairment (MCI). Methods: A comprehensive literature search was conducted across PubMed/Medline, Embase, and Scopus to identify relevant randomized controlled trials (RCTs) from inception to 20 August 2024. The search focused on comparing outcomes between intervention and control/placebo groups. Data searches, article selection, data extraction, and risk of bias assessment were performed in accordance with Cochrane guidelines. Systematic Review Registration: PROSPERO registration no: CRD42023446796. Results: Data from four RCTs involving 293 Individuals (AD and MCI patients) receiving mainly Lactobacillus and Bifidobacterium strains showed some beneficial effects on cognitive function, altered gut microbiota composition, and positively affected metabolic biomarkers. However, variability in microbiota assessment across studies limits the interpretation of results. The limited number and quality of the existing studies make it difficult to draw definitive conclusions from the data. Additional high-quality research is clearly needed. Conclusions: Probiotics show promise as an adjunctive intervention for cognitive decline, but larger, long-term trials are needed to confirm their efficacy and clinical applicability in neurodegenerative diseases like AD. Full article

Alcohol use disorder (AUD) affects millions of people worldwide and can lead to deleterious physical and social consequences. Recent research has highlighted not only the effect of alcohol on the gut microbiome, but also the role of the gut microbiome and the gut–brain axis in the development and maintenance of alcohol use disorder. This review provides an overview of the reciprocal relationship between alcohol consumption and the gut microbiome, including the effects of alcohol on gut microbial composition, changes in gut microbial metabolites in response to alcohol consumption, and how gut microbial metabolites may modulate alcohol use behavior. We also discuss the gut-mediated mechanisms of neuroinflammation that contribute to and result from AUD, including disruption of the intestinal barrier, toll-like receptor signaling, and the activation of glial cells and immune cells. Finally, we review the current evidence on gut microbial-directed therapies for AUD and discuss the implications of this research for our understanding of the pathophysiology of AUD and future research directions. Full article

Metabolic alterations, including hypermetabolism, lipid imbalances, and glucose dysregulation, are pivotal contributors to the onset and progression of Amyotrophic Lateral Sclerosis (ALS). These changes exacerbate systemic energy deficits, heighten oxidative stress, and fuel neuroinflammation. Simultaneously, gastrointestinal dysfunction and gut microbiota (GM) dysbiosis intensify disease pathology by driving immune dysregulation, compromising the intestinal barrier, and altering gut–brain axis (GBA) signaling, and lastly advancing neurodegeneration. Therapeutic and preventive strategies focused on nutrition offer promising opportunities to address these interconnected pathophysiological mechanisms. Diets enriched with antioxidants, omega-3 fatty acids, and anti-inflammatory compounds—such as the Mediterranean diet—have shown potential in reducing oxidative stress and systemic inflammation. Additionally, microbiota-targeted approaches, including probiotics, prebiotics, postbiotics, and fecal microbiota transplantation, are emerging as innovative tools to restore microbial balance, strengthen gut integrity, and optimize GBA function. This review highlights the critical need for personalized strategies integrating immunonutrition and microbiota modulation to slow ALS progression, improve quality of life, and develop preventive measures for neurodegenerative and neuroinflammatory diseases. Future research should prioritize comprehensive dietary and microbiota-based interventions to uncover their therapeutic potential and establish evidence-based guidelines for managing ALS and related disorders. Full article

Background/Objectives: Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons leading to debilitating motor and non-motor symptoms. Beyond its well-known neurological features, emerging evidence underscores the pivotal role of the gut–brain axis and gastrointestinal microbiota in PD pathogenesis. Dysbiosis has been strongly linked to PD and is associated with increased intestinal permeability, chronic inflammation, and the production of neurotoxic metabolites that may exacerbate neuronal damage. Methods: This review delves into the complex interplay between PD and dysbiosis, shedding light on two peculiar subsets of dysbiosis, Helicobacter pylori infection and small-intestinal bacterial overgrowth. These conditions may not only contribute to PD progression but also influence therapeutic responses such as L-dopa efficacy. Conclusions: The potential to modulate gut microbiota through probiotics, prebiotics, and synbiotics; fecal microbiota transplantation; and antibiotics represents a promising frontier for innovative PD treatments. Despite this potential, the current evidence is limited by small sample sizes and methodological variability across studies. Rigorous, large-scale, randomized placebo-controlled trials with standardized treatments in terms of composition, dosage, and duration are urgently needed to validate these findings and pave the way for microbiota-based therapeutic strategies in PD management. Full article

The gut–brain axis (GBA) is a complex communication network connecting the gastrointestinal tract (GIT) and the central nervous system (CNS) through neuronal, endocrine, metabolic, and immune pathways. Omega-3 (n-3) fatty acids, particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are crucial food components that may modulate the function of this axis through molecular mechanisms. Derived mainly from marine sources, these long-chain polyunsaturated fatty acids are integral to cell membrane structure, enhancing fluidity and influencing neurotransmitter function and signal transduction. Additionally, n-3 fatty acids modulate inflammation by altering eicosanoid production, reducing proinflammatory cytokines, and promoting anti-inflammatory mediators. These actions help preserve the integrity of cellular barriers like the intestinal and blood–brain barriers. In the CNS, EPA and DHA support neurogenesis, synaptic plasticity, and neurotransmission, improving cognitive functions. They also regulate the hypothalamic–pituitary–adrenal (HPA) axis by reducing excessive cortisol production, associated with stress responses and mental health disorders. Furthermore, n-3 fatty acids influence the composition and function of the gut microbiota, promoting beneficial bacterial populations abundance that contribute to gut health and improve systemic immunity. Their multifaceted roles within the GBA underscore their significance in maintaining homeostasis and supporting mental well-being. Full article

Neuroinflammation is a complex and dynamic response of the central nervous system (CNS) to injury, infection, and disease. While acute neuroinflammation plays a protective role by facilitating pathogen clearance and tissue repair, chronic and dysregulated inflammation contributes significantly to the progression of neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease, and Multiple Sclerosis. This review explores the cellular and molecular mechanisms underlying neuroinflammation, focusing on the roles of microglia, astrocytes, and peripheral immune cells. Key signaling pathways, including NF-κB, JAK-STAT, and the NLRP3 inflammasome, are discussed alongside emerging regulators such as non-coding RNAs, epigenetic modifications, and the gut–brain axis. The therapeutic landscape is evolving, with traditional anti-inflammatory drugs like NSAIDs and corticosteroids offering limited efficacy in chronic conditions. Immunomodulators, gene and RNA-based therapeutics, and stem cell methods have all shown promise for more specific and effective interventions. Additionally, the modulation of metabolic states and gut microbiota has emerged as a novel strategy to regulate neuroinflammation. Despite significant progress, challenges remain in translating these findings into clinically viable therapies. Future studies should concentrate on integrated, interdisciplinary methods to reduce chronic neuroinflammation and slowing the progression of neurodegenerative disorders, providing opportunities for revolutionary advances in CNS therapies. Full article

Developmental exposure to benzo[a]pyrene (BaP), a ubiquitous environmental pollutant, has been linked to various toxic effects, including multigenerational behavioral impairment. While the specific mechanisms driving BaP neurotoxicity are not fully understood, recent work highlights two important determinants of developmental BaP neurotoxicity: (1) the aryl hydrocarbon receptor (AHR), which induces host metabolism of BaP, and (2) the gut microbiome, which may interact with BaP to affect its metabolism, or be perturbed by BaP to disrupt the gut–brain axis. We utilized the zebrafish model to explore the role of AHR, the gut microbiome, and their interaction, on BaP-induced neurotoxicity. We tested (1) how developmental BaP exposure and AHR2 perturbation in zebrafish link to adult behavior, (2) how these variables associate with the structure and function of the adult zebrafish gut metagenome, and (3) whether these associations are multigenerational. Our findings reveal a reticulated axis of association between BaP exposure, developmental AHR2 expression, the zebrafish gut metagenome, and behavior. Results indicate that AHR2 is a key modulator of how BaP elicits neurotoxicity and microbiome dysbiosis. Additionally, this axis of association manifests generationally. These findings demonstrate the importance of studying pollutant–microbiome interactions and elucidate the role of specific host genes in neurotoxicity and dysbiosis. Full article

The human microbiota constitute a very complex ecosystem of microorganisms inhabiting both the inside and outside of our bodies, in which health maintenance and disease modification are the main regulatory features. The recent explosion of microbiome research has begun to detail its important role in neurological health, particularly concerning cerebral small vessel disease (CSVD), a disorder associated with cognitive decline and vascular dementia. This narrative review represents state-of-the-art knowledge of the intimate, complex interplay between microbiota and brain health through the gut–brain axis (GBA) and the emerging role of glymphatic system dysfunction (glymphopathy) and circulating cell-derived microparticles (MPs) as mediators of these interactions. We discuss how microbial dysbiosis promotes neuroinflammation, vascular dysfunction, and impaired waste clearance in the brain, which are critical factors in the pathogenesis of CSVD. Further, we discuss lifestyle factors that shape the composition and functionality of the microbiota, focusing on sleep as a modifiable risk factor in neurological disorders. This narrative review presents recent microbiome research from a neuroscientific and vascular perspective to establish future therapeutic avenues in targeting the microbiota to improve brain health and reduce the burden of CSVD. Full article

Background: Recent studies indicate the need to examine how the gut microbiota–brain axis is implicated in pain, sensory reactivity and gastro-intestinal symptoms in autism spectrum disorder (ASD), but no scale exists that assesses all these constructs simultaneously. Methods: We created a pool of 100 items based on the real-world experience of autistic people, and a multidisciplinary team and stakeholders reduced this pool to 50 items assessing pain, sensory hypersensitivity, and sensory hyposensitivity. In the present study, we present this new assessment tool, the Pain and Sensitivity Reactivity Scale (PSRS), and examine its psychometric properties in a sample of 270 individuals with autism spectrum disorder (ASD; mean age = 9.44, SD = 4.97), of which almost half (45%) had intellectual disability (ID). Results: A factorial model of three factors (pain, hyporeactivity, and hyperreactivity) and five specific factors for sensory hypo- and hyperreactivity, respectively, fitted the data well. Good to excellent internal consistency and adequate test–retest reliability was found for most PSRS scales. Sound psychometric properties were found in individuals with and without ID. Correlations with other measures of sensory sensitivity and pain indicated sound convergent validity. Conclusions: PSRS shows promise as a reliable measure to analyze pain and sensory reactivity in autistic people regardless of whether they have ID or not. The measure overcomes several limitations of previous assessment tools and includes variables that are important for the understanding of the gut microbiota–brain axis in ASD. Full article

Radiation therapy is widely recognized as an efficacious modality for treating neoplasms located within the craniofacial region. Nevertheless, this approach is not devoid of risks, predominantly concerning potential harm to the neural structures. Adverse effects may encompass focal cerebral necrosis, cognitive function compromise, cerebrovascular pathology, spinal cord injury, and detriment to the neural fibers constituting the brachial plexus. With increasing survival rates among oncology patients, evaluating post-treatment quality of life has become crucial in assessing the benefits of radiation therapy. Consequently, it is imperative to investigate therapeutic strategies to mitigate cerebral complications from radiation exposure. Current management of radiation-induced cerebral damage involves corticosteroids and bevacizumab, with preclinical research on antioxidants and thalidomide. Despite these efforts, an optimal treatment remains elusive. Recent studies suggest the gut microbiota’s involvement in neurologic pathologies. This review aims to discuss the causes and existing treatments for radiation-induced cerebral injury and explore gut microbiota modulation as a potential therapeutic strategy. Full article

The gut–brain axis plays an integral role in maintaining overall health, with growing evidence suggesting its impact on the development of various neuropsychiatric disorders, including depression. This review explores the complex relationship between gut microbiota and glutamate (Glu) regulation, highlighting its effect on brain health, particularly in the context of depression following certain neurological insults. We discuss how microbial populations can either facilitate or limit Glu uptake, influencing its bioavailability and predisposing to neuroinflammation and neurotoxicity. Additionally, we examine the role of gut metabolites and their influence on the blood–brain barrier and neurotransmitter systems involved in mood regulation. The therapeutic potential of microbiome-targeted interventions, such as fecal microbiota transplantation, is also highlighted. While much research has explored the role of Glu in major depressive disorders and other neurological diseases, the contribution of gut microbiota in post-neurological depression remains underexplored. Future research should focus on explaining the mechanisms linking the gut microbiota to neuropsychiatric outcomes, particularly in conditions such as post-stroke depression, post-traumatic brain-injury depression, and epilepsy-associated depression. Systematic reviews and human clinical studies are needed to establish causal relationships and assess the efficacy of microbiome-targeted therapies in improving the neuropsychiatric sequalae after neurological insults. Full article

Aim: This article aims to explore the role of the human gut microbiota (GM) in the pathogenesis of neurological, psychiatric, and neurodevelopmental disorders, highlighting its influence on health and disease, and investigating potential therapeutic strategies targeting GM modulation. Materials and Methods: A comprehensive analysis of the gut microbiota’s composition and its interaction with the human body, particularly, its role in neurological and psychiatric conditions, is provided. The review discusses factors influencing GM composition, including birth mode, breastfeeding, diet, medications, and geography. Additionally, it examines the GM’s functions, such as nutrient absorption, immune regulation, and pathogen defense, alongside its interactions with the nervous system through the gut–brain axis, neurotransmitters, and short-chain fatty acids (SCFAs). Results: Alterations in the GM are linked to various disorders, including Parkinson’s disease, multiple sclerosis, depression, schizophrenia, ADHD, and autism. The GM influences cognitive functions, stress responses, and mood regulation. Antibiotic use disrupts GM diversity, increasing the risk of metabolic disorders, obesity, and allergic diseases. Emerging therapies such as probiotics, prebiotics, and microbiota transplantation show promise in modulating the GM and alleviating symptoms of neurological and psychiatric conditions. Conclusions. The modulation of the GM represents a promising approach for personalized treatment strategies. Further research is needed to better understand the underlying mechanisms and to develop targeted therapies aimed at restoring GM balance for improved clinical outcomes. Full article

Irritable bowel syndrome (IBS) is a functional gastrointestinal disorder (FGID) characterized by chronic or recurrent gastrointestinal symptoms without organic changes, and it is also a common disorder of gut–brain interaction (DGBIs).. The symptoms of IBS not only affect the quality of life for individual patients but also place a significant burden on global healthcare systems. The lack of established and universally applicable biomarkers for IBS, along with the substantial variability in symptoms and progression, presents challenges in developing effective clinical treatments. In recent years, preclinical and clinical studies have linked the pathogenesis of IBS to alterations in the composition and function of the intestinal microbiota. Within the complex microbial community of the gut, intricate metabolic and spatial interactions occur among its members and between microbes and their hosts. Amid the multifaceted pathophysiology of IBS, the role of intestinal microenvironment factors in symptom development has become more apparent. This review aims to delve into the changes in the composition and structure of the gut microbiome in individuals with IBS. It explores how diet-mediated alterations in intestinal microbes and their byproducts play a role in regulating the pathogenesis of IBS by influencing the “brain-gut” axis, intestinal barrier function, immune responses, and more. By doing so, this review seeks to lay a theoretical foundation for advancing the development of clinical therapeutics for IBS. Full article

The gut microbiota, a complex ecosystem, is vital to host health as it aids digestion, modulates the immune system, influences metabolism, and interacts with the brain-gut axis. Various factors influence the composition of this microbiota. Enzymes, as essential catalysts, actively participate in biochemical reactions that have an impact on the gut microbial community, affecting both the microorganisms and the gut environment. Enzymes play an important role in the regulation of the intestinal microbiota, but the interactions between enzymes and microbial communities, as well as the precise mechanisms of enzymes, remain a challenge in scientific research. Enzymes serve both traditional nutritional functions, such as the breakdown of complex substrates into absorbable small molecules, and non-nutritional roles, which encompass antibacterial function, immunomodulation, intestinal health maintenance, and stress reduction, among others. This study categorizes enzymes according to their source and explores the mechanistic principles by which enzymes drive gut microbial activity, including the promotion of microbial proliferation, the direct elimination of harmful microbes, the modulation of bacterial interaction networks, and the reduction in immune stress. A systematic understanding of enzymes in regulating the gut microbiota and the study of their associated molecular mechanisms will facilitate the application of enzymes to precisely regulate the gut microbiota in the future and suggest new therapeutic strategies and dietary recommendations. In conclusion, this review provides a comprehensive overview of the role of enzymes in modulating the gut microbiota. It explores the underlying molecular and cellular mechanisms and discusses the potential applications of enzyme-mediated microbiota regulation for host gut health. Full article

Emerging evidence underscores the pivotal role of the gut microbiota in regulating emotional and behavioral responses via the microbiota–gut–brain axis. This study explores associations between pediatric obstructive sleep apnea (OSA), emotional distress (ED), and gut microbiome alterations before and after OSA treatment. Sixty-six children diagnosed with OSA via polysomnography participated, undergoing adenotonsillectomy alongside routine educational sessions. ED was assessed using the OSA-18 questionnaire, categorizing participants into high ED (scores ≥ 11, 52%) and low ED (scores < 11, 48%) groups. Gut microbiome analysis revealed significant diversity differences, with high ED linked to a reduced Shannon index (p = 0.03) and increased beta diversity (p = 0.01). Three months post-treatment, significant improvements were observed in OSA symptoms, ED scores, and gut microbiome alpha diversity metrics among 55 participants (all p < 0.04). Moreover, changes in the relative abundances of Veillonella, Bifidobacterium, Flavonifractor, and Agathobacter, as well as ultra-low frequency power and low frequency power of sleep heart rate variability, were independently associated with ED score alterations. These findings underscore the gut microbiome’s critical role in the emotional and behavioral symptoms associated with pediatric OSA, suggesting that microbiome-targeted interventions could complement traditional treatments for ED reduction and emphasizing the need for further research. Full article