Search Results (517)

Parkinson’s disease (PD), the second most common neurodegenerative disorder globally, relies primarily on dopamine replacement therapy for conventional treatment. This approach fails to reverse core pathological processes and is associated with long-term side effects. Recent research on the microbiota-gut-brain axis (MGBA) has revealed that PD pathology may originate in the gut, forming a vicious cycle from the gut to brain through α-synuclein propagation, gut dysbiosis, intestinal barrier disruption, and neuroinflammation. This offers a novel perspective for managing PD through dietary interventions that modulate the gut microbiome. However, single probiotic or prebiotic interventions show limited efficacy. This review systematically introduces the novel concept of “synbiotics combining medicinal plant polysaccharides with probiotics,” aiming to integrate traditional “medicinal food” wisdom with modern microbiome science. The article systematically elucidates the pathological mechanisms of MGBA dysfunction in PD and the intervention mechanisms of probiotics and emphasizes the structural and functional advantages of medicinal plant polysaccharide as superior prebiotics. The core section delves into the multifaceted synergistic mechanisms between these two components: enhancing probiotic colonization and vitality, optimizing microbial metabolic output, synergistically reinforcing the intestinal and blood-brain barriers, and jointly regulating immune and neuroinflammation. This approach targets the MGBA to achieve multi-level intervention for PD. Full article

The gut microbiota has emerged as a central regulator of the gut–brain axis, profoundly influencing neural, immune, and metabolic homeostasis. Increasing evidence indicates that disturbances in microbial composition and function contribute to the onset and progression of neurodegenerative diseases (NDs) through mechanisms involving neuroinflammation, oxidative stress, and impaired neurotransmission. Gut dysbiosis is characterized by a loss of microbial diversity, a reduction in beneficial commensals, and an enrichment of pro-inflammatory taxa. These shifts alter intestinal permeability and systemic immune tone, allowing microbial metabolites and immune mediators to affect central nervous system (CNS) integrity. Metabolites such as short-chain fatty acids (SCFAs), tryptophan derivatives, lipopolysaccharides (LPS), and trimethylamine N-oxide (TMAO) modulate blood–brain barrier (BBB) function, microglial activation, and neurotransmitter synthesis, linking intestinal imbalance to neuronal dysfunction and cognitive decline. Disruption of this gut–brain communication network promotes chronic inflammation and metabolic dysregulation, key features of neurodegenerative pathology. SCFA-producing and tryptophan-metabolizing bacteria appear to exert neuroprotective effects by modulating immune responses, epigenetic regulation, and neuronal resilience. The aim of this work was to comprehensively explore the current evidence on the bidirectional communication between the gut microbiota and the CNS, with a focus on identifying the principal molecular, immune, and metabolic mechanisms supported by the strongest and most consistent data. By integrating findings from recent human studies, this review sought to clarify how microbial composition and function influence neurochemical balance, immune activation, and BBB integrity, ultimately contributing to the onset and progression of neurodegenerative processes. Collectively, these findings position the gut microbiota as a dynamic interface between the enteric and CNS, capable of influencing neurodegenerative processes through immune and metabolic signaling. Full article

Background: Growing evidence indicates that oral microbiome dysbiosis contributes to systemic inflammation, immune activation, and neural dysfunction. These processes may influence the onset and progression of major neuropsychiatric and neurodegenerative disorders. This review integrates clinical, epidemiological, and mechanistic findings linking periodontal pathogens and oral microbial imbalance to Alzheimer’s disease (AD), Parkinson’s disease (PD), depression, and anxiety. Methods: A narrative review was conducted using PubMed/MEDLINE, Scopus, Web of Science, and Google Scholar to identify recent studies examining alterations in the oral microbiota, microbial translocation, systemic inflammatory responses, blood–brain barrier disruption, cytokine signaling, and neural pathways implicated in brain disorders. Results: Evidence from human and experimental models demonstrates that oral pathogens, particularly Porphyromonas gingivalis, Fusobacterium nucleatum, and Treponema denticola, can disseminate systemically, alter immune tone, and affect neural tissues. Their virulence factors promote microglial activation, cytokine release (IL-1β, IL-6, TNF-α), amyloid-β aggregation, and α-synuclein misfolding. Epidemiological studies show associations between oral dysbiosis and cognitive impairment, motor symptoms in PD, and alterations in mood-related taxa linked to stress hormone profiles. Immunometabolic pathways, HPA-axis activation, and the oral–gut–brain axis further integrate these findings into a shared neuroinflammatory framework. Conclusions: Oral dysbiosis emerges as a modifiable contributor to neuroinflammation and brain health. Periodontal therapy, probiotics, prebiotics, synbiotics, and targeted inhibitors of bacterial virulence factors represent promising strategies to reduce systemic and neural inflammation. Longitudinal human studies and standardized microbiome methodologies are still needed to clarify causality and evaluate whether restoring oral microbial balance can modify the course of neuropsychiatric and neurodegenerative disorders. Full article

Background: Unhealthy diets characterized by high salt, fat, and fructose content are established risk factors for metabolic and cardiovascular disorders and may have indirect effects on cognitive function. However, the combined impact of a high-salt, high-fat, and high-fructose diet (HSHFHFD) on systemic physiology and brain health remains to be fully elucidated. Methods: Sprague-Dawley (SD) rats received a customized high-salt, high-fat diet supplemented with 30% fructose water for 18 weeks. Physiological and brain parameters were assessed, in combination with multi-omics analyses including brain proteomics and metabolomics, serum metabolomics, and gut microbiota profiling. Results: HSHFHFD significantly elevated blood glucose, blood pressure, and serum levels of TG, TC, and LDL in rats. Serum metabolomic profiling identified over 100 differentially abundant metabolites in the Model group. Proteomics, metabolomics, and gut microbiome integration revealed pronounced alterations in both brain proteomic and metabolomic profiles, with 155 differentially expressed proteins associated with glial cell proliferation and 65 differential metabolites linked to fatty acid and amino acid metabolism, among others. Experimental validation confirmed marked upregulation of GFAP and Bax protein, concomitant with downregulation of ZO-1 and occludin. Furthermore, HSHFHFD perturbed the CREB signaling pathway, leading to diminished BDNF expression. The levels of inflammatory factors, including IL-6, IL-10, IL-1β and TNFα, were significantly elevated in the brain. Oxidative stress was evident, as indicated by elevated malondialdehyde (MDA) levels, increased superoxide dismutase (SOD) activity, and altered NAD⁺/NADH ratio. Additionally, HSHFHFD significantly reduced the abundance of beneficial gut bacteria, including Lactobacillus, Romboutsia, and Monoglobus. Conclusions: HSHFHFD-induced depletion of gut Lactobacillus spp. may disrupt the linoleic acid metabolic pathway and gut–brain axis homeostasis, leading to the impairment of neuroprotective function, blood–brain barrier dysfunction, and exacerbated neuroinflammation and oxidative stress in the brain. These effects potentially increase the susceptibility of rats to neurodegenerative disorders. Full article

Background: Parkinson’s disease (PD) involves progressive neurodegeneration with clinical or subclinical disturbance of the gut–brain axis, including altered gastrointestinal motility and enteric nervous system involvement. Clinical studies have reported gut microbiome alterations in PD, with shifts in taxa associated with inflammatory signalling and short-chain fatty acid (SCFA) metabolism. Photobiomodulation (PBM), a non-invasive light therapy, has been investigated as a potential adjunctive treatment for PD, with proposed effects on neural, metabolic, and immune pathways. We previously reported the five-year clinical outcomes in a PBM-treated Parkinson’s disease case series. Here we report the five-year gut microbiome outcomes based on longitudinal samples collected from the same participants. This was an exploratory, open-label longitudinal study without a control group. Objective: Our objective was to assess whether long-term PBM was associated with changes in gut microbiome diversity and composition in the same Parkinson’s disease cohort as previously assessed for changes in Parkinson’s symptoms. Methods: Six participants from the earlier PBM proof-of-concept study who had been diagnosed with idiopathic PD and who had continued treatment (transcranial light emitting diode [LED] plus abdominal and neck laser) for five years had their faecal samples analysed by 16S rDNA sequencing to assess microbiome diversity and taxonomic composition. Results: Microbiome analysis revealed significantly reduced evenness (α-diversity) and significant shifts in β-diversity over five years, as assessed by Permutational Multivariate Analysis of Variance (PERMANOVA). At the phylum level, Pseudomonadota and Methanobacteriota decreased in four of the six participants. Both of these phyla are often increased in the Parkinson’s microbiome compared with the microbiomes of healthy controls. Family-level changes included increased acetate-producing Bifidobacteriaceae (five of the six participants); decreased pro-inflammatory, lipopolysaccharide (LPS)-producing Enterobacteriaceae (two of the three participants who have this bacterial family present); and decreased LPS- and H₂S-producing Desulfovibrionaceae (five of six). At the genus level, Faecalibacterium, a key butyrate producer, increased in four of the six participants, potentially leading to more SCFA availability, although other SCFA-producing bacteria were decreased. This was accompanied by reductions in pro-inflammatory LPS and H₂S-producing genera that are often increased in the Parkinson’s microbiome. Conclusions: This five-year case series represents the longest follow-up of microbiome changes in Parkinson’s disease, although the interpretation of results is limited by very small numbers, the lack of a control group, and the inability to control for lifestyle influences such as dietary changes. While causal relationships cannot be inferred, the parallel changes in improvements in mobility and non-motor Parkinson’s symptoms observed in this cohort, raises the hypothesis that PBM may interact with the gut–brain axis via the microbiome. Controlled studies incorporating functional multi-omics are needed to clarify potential mechanistic links between microbial function, host metabolism, and clinical outcomes. Full article

Medium- and long-chain fatty acids (MLFAs) are increasingly recognized not only as metabolic substrates but also as precursors of diverse bioactive metabolites generated through host and microbial transformations. Recent advances in analytical chemistry and microbiome research have revealed that gut microorganisms catalyze extensive modifications of dietary MLFAs—producing hydroxylated, conjugated, and keto-fatty acids with enhanced potency toward host receptors. These metabolites exhibit dual activity on classical metabolic receptors, including FFAR1/4 and PPARα/γ, as well as ectopically expressed chemosensory receptors such as olfactory receptors (ORs) and bitter taste receptors (TAS2Rs). This expanded receptor landscape establishes a previously unrecognized chemosensory–metabolic axis that integrates dietary signals, microbial metabolism, and host physiology. Microbial MLFA derivatives such as 10-hydroxyoctadecenoic acid and conjugated linoleic acid regulate incretin secretion, adipogenesis, macrophage polarization, and intestinal barrier function through coordinated activation of FFARs and PPARs. Concurrently, dicarboxylic acids such as azelaic acid activate Olfr544 to modulate lipolysis, ketogenesis, GLP-1 release, and feeding behavior. TAS2Rs also sense oxidized lipids, linking lipid metabolism to immune regulation and enteroendocrine signaling. Collectively, these pathways highlight the microbiome as a metabolic transducer that converts dietary lipids into signaling molecules influencing endocrine, immune, and gut–brain circuits. Understanding the mechanisms governing MLFA bioconversion and receptor engagement provides new opportunities for therapeutic and nutritional intervention. Targeting ORs and TAS2Rs, engineering probiotics to enhance beneficial FA-derived metabolites, and developing receptor-selective synthetic analogs represent promising strategies. Future progress will require integrative approaches combining physiology, biochemistry, metabolomics, and microbial genomics to elucidate receptor specificity and host variability. Full article

Growing evidence has revealed that gut dysbiosis is associated with the development of anxio-depressive disorders through mechanisms that involve neuroimmune signaling, neurotransmitter changes, and neuroplasticity in the brain. This study investigated the effects of gingerol-enriched ginger (GEG) on specifically anxiety-related neuroinflammation-, neuroimmunity-, neuroplasticity-, neurotransmission-, and neurotoxicity-associated genes in different brain regions, as well as on alterations linked to colonic microflora-driven dysbiosis, in the spinal nerve ligation (SNL) rat model of neuropathic pain (NP). Twenty-seven male rats were assigned to 3 groups: sham, SNL, and SNL-treated with GEG at 200 mg/kg body weight (SNL+200GEG) via oral gavage for 5 weeks. Anxiety-like behavior was assessed on the elevated plus maze (EPM). mRNA expression was assessed by qRT-PCR using respective primers. Correlation between behavioral parameters and colonic microbiome composition was analyzed using the Spearman rank correlation. The SNL+200GEG group demonstrated decreased anxiety-like behavior in the SNL model. Compared to the SNL group, the SNL+200GEG group had increased mRNA expression of NRF2 (amygdala: left), LXRα (amygdala: both sides), and CX3CR1 (amygdala: both sides, hippocampus: right). GEG modulated neuroplasticity as shown by increased gene expression of PGK1 (amygdala: right, hippocampus: both sides), MEK1 (frontal cortex: both sides), LDHA (frontal cortex: both sides), GPM6A (frontal cortex: both sides, amygdala: right, hippocampus: right, and hypothalamus), and GLUT1 (amygdala: right) as well by decreased gene expression of HIF1α (in all brain regions except for the hypothalamus). GEG modulated neurotransmission via clearance of excessive glutamate release as suggested by increased gene expression of SLC1A3 (frontal cortex: both sides, hippocampus: right) and via augmenting mGluR5 signaling as shown by increased gene expression of GRM5 (hippocampus: both sides, hypothalamus) as well as downregulation of KMO, HAAO, GRIN2B, and GRIN2C influencing downstream serotonergic neurotransmission and NMDA receptor-mediated glutamatergic pathways in different brain regions. GEG further alleviated neurotoxicity through downregulated gene expression of SIRT1, KMO, IDO1, and HAAO in different brain regions. Moreover, the increased relative abundance of Bilophila spp., accompanied by decreased time spent in the EPM open arms, suggests that increased Bilophila abundance increases anxiety-like behavior. GEG supplementation mitigated anxiety-like behavior in male rats with NP, at least in part, by reducing SNL-induced inflammatory sequelae-related mRNA gene expression in different brain regions. In addition, there is a positive correlation between the abundance of Bilophila wadsworthia and the degree of anxiety-like behavior. Full article

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a disabling clinical condition, whose hallmark characteristic is post-exertional malaise (PEM). It can affect many organs and systems, leading to severe impairment of patients’ quality of life. Although numerous post-infectious, immunological, neurological, metabolic, and endocrine alterations have been documented, neither a definitive diagnostic marker nor approved treatments are available. The etiology and pathophysiology remain incompletely understood; however, emerging evidence suggests that the gut microbiome plays a role in immune responses and the development of ME/CFS. It is hypothesized that specific disturbances in gut microbiome composition, known as dysbiosis, may compromise the integrity of the intestinal barrier. This consequently leads to translocation of microbial components, which further triggers an immune response and systemic inflammation complicating the clinical presentation of ME/CFS. Furthermore, in terms of the so-called gut–brain axis, microbiome changes may lead to distinct neurocognitive impairments observed in ME/CFS patients. This review offers the readers a broad perspective on the topic on ME/CFS, with a particular emphasis on the interplay between the gut microbiome and disease mechanisms. Last but not least, recent data on potential treatment strategies for intestinal dysbiosis in ME/CFS patients have been included. Full article

The intestinal microbiota, a diverse community of microorganisms residing in the human gut, recently attracted considerable attention as a contributing factor to various neurological disorders, including Alzheimer’s Disease (AD). Within the established framework of the gut–brain axis (GBA) concept, it is commonly suggested that dysbiosis, through microbial metabolites entering the brain, affect the cognitive functions in patients with AD. However, evidence for such a role of dysbiosis remains largely associative, and the complexity of the communication channels between the gut and the brain is not fully understood. Moreover, the new players of the GBA are emerging and the AD concept is constantly evolving. The objective of this narrative review is to synthesize the current evidence on the humoral, endocrine, immune, and neural communication mechanisms linking the gut and brain in AD and highlight newly discovered GBA messengers such as microRNAs, extracellular vesicles, T-cells, and the intestinal hormones, including emerging neuroprotective role for glucagon-like peptide-1 (GLP-1). Based on this knowledge, we aimed to develop a conceptual understanding of the GBA function in health and AD. We specify that, in AD, the GBA goes beyond a disrupted microbiome, but operates in conjunction with impaired intestinal secretion, motility, barrier permeability, and neuroinflammatory signaling. These factors are associated with the dysfunction of the hypothalamic–pituitary axis, altered somatic and autonomic neuronal gut regulation, and abnormal, due to memory problems, behavioral aspects of food intake. Identifying the individual profile of key molecular and cellular players contributing to an unbalanced GBA should optimize existing approaches or propose new approaches for the complex therapy of AD. Full article

Background/Objectives: Nutritional patterns influence the gut–brain axis and immune signaling with potential consequences for depression and anxiety. We conducted a review focused on clinically meaningful psychiatric outcomes (symptom severity/diagnosis) to synthesize recent evidence (2020–2025) on Mediterranean-style dietary interventions; ultra-processed food (UPF) exposure; and psychobiotic/prebiotic strategies, integrating mechanistic insights relevant to practice. Methods: Searches in PubMed/MEDLINE, Scopus, and Web of Science (January 2020–October 2025) combined terms for diet, Mediterranean diet (MD), UPF, microbiota, probiotics, psychobiotics, depression, and anxiety. Eligible designs were randomized/controlled trials (RCTs), prospective cohorts, and systematic reviews/meta-analyses reporting clinical psychiatric outcomes in adults. We prioritized high-quality quantitative syntheses and recent RCTs; data were extracted into a prespecified matrix and synthesized narratively. Results: Recent systematic reviews/meta-analyses support that MD interventions reduce depressive symptoms in adults with major or subthreshold depression, although large, long-term, multicenter RCTs remain a gap. Exposure to UPF is consistently associated with higher risk of common mental disorders and depressive outcomes in large prospective cohorts. Psychobiotics (specific probiotic strains and prebiotics) show small-to-moderate benefits on depressive symptoms across clinical and nonclinical samples, with heterogeneity in strains, dosing, and duration. Mechanistic reviews implicate microbiota-derived metabolites (short-chain fatty acids) and immune–inflammatory signaling (including tryptophan–kynurenine pathways) as plausible mediators. Conclusions: Clinically, emphasizing Mediterranean-style dietary patterns, reducing UPF intake, and considering targeted psychobiotics may complement standard psychiatric care for depression. Future work should prioritize adequately powered, longer RCTs with standardized dietary protocols and microbiome-informed stratification to clarify responders and mechanisms. Full article

Probiotics have been increasingly evaluated for their potential effect on anxiety and depression through the modulation of the gut–brain axis. Individuals with cancer experience a high prevalence of these symptoms. However, the effects of probiotics and their underlying mechanisms in this population have not been systematically evaluated. This review synthesizes current evidence regarding probiotic interventions for anxiety and depression in cancer and examines the associated mechanistic pathways. A systematic search for original trials in PubMed, Embase, CINAHL, Web of Science, and PsycINFO was conducted in May 2025. Eligible studies included animal models or adults with cancer who received probiotics alone or in combination with other treatments, with outcomes related to anxiety, depressive symptoms, or depression. Search terms included animal model, cancer, probiotics, anxiety, depressive symptoms, depression, gastrointestinal microbiome, gut microbiome, and microbiota. The review followed PRISMA guidelines. Risk of bias in trials was assessed using the SYRCLE and Cochrane RoB2 tool. Nine studies met the inclusion criteria, including seven human studies, one animal study, and one mixed human–animal study, with human sample sizes ranging from 24 to 266. The animal study reported reductions in depressive and anxiety-like behaviors, paralleled by modulation of the hypothalamic–pituitary–adrenal (HPA) axis, reduced inflammation, rebalancing of the gut microbiota, and improvements in neurotransmitter pathways. Findings from human studies were more variable. Some trials reported improvements in anxiety, and depressive symptoms, while others showed no significant differences compared with control groups. Studies that combined probiotics with antidepressants or exercise demonstrated the most pronounced reductions in anxiety and depression. Mechanistic insights from human studies partially aligned with animal evidence, with several trials showing reductions in inflammatory markers (IL-6, TNF-α), improvements in neuroendocrine measures (serotonin, dopamine, cortisol), stabilization of metabolic markers, and favorable shifts in gut microbiota, although these effects were not consistent across all studies. Probiotics appear to be safe within the intervention periods of the reviewed studies (<24 weeks), as no serious adverse effects were reported. Substantial heterogeneity across studies, including variations in cancer type, intervention duration, probiotic strains, formulations, dosages, and study design combined with small sample sizes, restricts the ability to draw definitive conclusions. Rigorously designed randomized controlled trials with larger sample sizes and mechanistic biomarkers are required to confirm the efficacy of probiotics for relieving anxiety and depression in the cancer population. Full article

Background and Objectives: Fibromyalgia (FM) is associated with chronic pain, oxidative stress, low-grade inflammation, and disturbances in signalling along the gut–brain axis. These pathways may be modulated by plant-derived phytonutrients. This narrative review summarises mechanistic and clinical evidence on phytonutrient-based strategies in FM. Materials and Methods: Following SANRA guidelines, we searched PubMed, Web of Science, Scopus and ScienceDirect for human and relevant preclinical studies published between 2005 and October 2025 that evaluated phytonutrient-rich dietary patterns or isolated bioactives in relation to FM symptoms or underlying mechanisms. Results: There is a consistent association between FM and increased oxidative damage and reduced antioxidant defences. Adopting plant-based diets, particularly Mediterranean-type and low-FODMAP diets, has been linked to improvements in pain, fatigue, sleep, and gastrointestinal symptoms, as well as modest gains in quality of life. However, the effects on inflammatory markers are conflicting. Trials of selected bioactive compounds, such as coenzyme Q10, curcumin-based formulations, L-carnitine and certain probiotics, suggest beneficial effects on symptoms, whereas others show little or no effect. Studies of the microbiome indicate a loss of butyrate-producing bacteria and altered microbial metabolites. Early dietary or probiotic interventions may partially mitigate these changes to some extent. Preclinical studies have identified SIRT1 as a potential mediator, but there is a lack of human data. Reporting on safety, dosage and formulation is often inadequate. Conclusions: Given the narrative design of this review and the methodological heterogeneity of the included studies, the overall certainty of the evidence cannot be formally graded and should be regarded as limited and heterogeneous. Nevertheless, current data supports phytonutrient-rich, food-based approaches as adjuncts rather than alternatives to standard FM care. Well-designed randomised trials with standardised outcomes and reporting of dose, formulation and relevant biomarkers are needed to identify the most effective strategies and the patient subgroups most likely to benefit. Full article

Disruption of the gut-microbiome-brain axis contributes to the development of chronic inflammation, impaired intestinal barrier integrity, and progressive tissue damage, ultimately reducing quality of life and increasing risk of comorbidities, including neurodegenerative diseases. Current therapies are often limited by adverse effects and insufficient long-term efficacy, highlighting the need for more comprehensive therapeutic approaches. Berberine (BRB), a plant-derived isoquinoline alkaloid, has attracted growing attention due to its pleiotropic immunomodulatory, neuroprotective, and gut-homeostasis-modulating properties, which involve reshaping the gut microbiota and underscore its therapeutic relevance within the gut–microbiome–brain axis. The aim of this review is to synthesize current scientific evidence regarding the anti-inflammatory mechanisms of BRB in inflammatory bowel disease (IBD). We compare its activity with first-line therapies and discuss its impact on microbial composition, including the bidirectional regulation of specific bacterial taxa relevant to intestinal and systemic disorders that originate in the gut. Furthermore, we emphasize that gut bacteria convert BRB into bioactive metabolites, contributing to its enhanced intraluminal activity despite its low systemic bioavailability. By integrating molecular and microbiological evidence, this review fills a critical knowledge gap regarding the comprehensive therapeutic potential of BRB as a promising candidate for future IBD interventions. The novelty of this work lies in unifying fragmented findings into a framework that explains how BRB acts simultaneously at the levels of host immunity, microbial ecology, and neuroimmune communication—thus offering a new conceptual model for its role within the gut–microbiome–brain axis. Full article

Background/Objectives: Bidirectional communication between the gut and brain is central to neurological and psychiatric health, and abdominal photobiomodulation (PBM) has emerged as a promising non-invasive way to modulate this axis by targeting intestinal mitochondria, epithelial integrity, and the microbiota. We systematically reviewed preclinical and clinical evidence on abdominal PBM, alone or in combined protocols, reporting microbiome, metabolic, or neurobehavioral outcomes. Methods: Following PRISMA 2020 recommendations, we searched MEDLINE, Scopus, Web of Science, and ScienceDirect through May 2025 for animal and human studies applying PBM to the abdomen and reporting gut-related, metabolic, or brain-related outcomes. Results: Nine studies met the eligibility criteria (five human, four animal). Human trials, mainly in Parkinson’s and Alzheimer’s disease, used 630–904 nm light and reported gains in mobility, balance, cognition, and olfaction; one trial also showed microbiota modulation with a decreased Firmicutes:Bacteroidetes ratio. Animal models revealed cognitive improvement, reduced neuroinflammation, dopaminergic neuroprotection, and microbial rebalancing. Mechanistic findings converged on enhanced mitochondrial bioenergetics, redox and anti-inflammatory signaling, vagal activation, and short-chain fatty acid-mediated effects. Conclusions: Current evidence, though limited by small samples, heterogeneous dosimetry, combined treatment sites, and few sham-controlled human trials, suggests that abdominal PBM can influence the gut–brain axis through converging mitochondrial, immune, and microbial mechanisms. Adequately powered randomized trials with standardized dosimetry, validated mechanistic biomarkers, and integrative multi-omics analyses are needed to clarify causal pathways and optimize translational applications. Full article

Background: Hearing loss (HL) affects more than 1.5 billion people worldwide and represents a major global health concern. Recent evidence suggests that alterations in gut microbial composition and antimicrobial resistance (AMR) may be linked to inflammatory and metabolic pathways that could influence auditory physiology. Objectives: This study aimed to explore the relationship between auditory function and the antimicrobial resistance in the gut microbiome of young adults. Methods: Fecal and auditory data were collected from young adults. Auditory function was assessed through pure-tone audiometry, and participants were classified according to the presence or absence of HL based on the American Speech-Language-Hearing Association (ASHA) criteria. Bacterial resistance was analyzed under aerobic and anaerobic conditions using disk diffusion and E-test methods to determine minimum inhibitory concentrations (MICs) for a panel of antibiotics. Gut microbiota composition was further characterized using quantitative polymerase chain reaction (qPCR) to quantify 15 key microbial taxa. Results: Overall, 40.9% of participants presented some degree of HL, with mild or slight HL being more frequent in women (53.3%) than in men (14.3%). Participants with HL exhibited significantly higher MICs for nalidixic acid, amoxicillin, and ciprofloxacin, as well as trends toward increased MIC variability for several other agents. Principal component analysis demonstrated distinct clustering of individuals without HL and greater dispersion among those with HL, suggesting higher interindividual variability in resistance profiles. These findings suggest potential associations between antimicrobial resistance and auditory function, possibly mediated through gut microbiome alterations. qPCR analyses demonstrated that Faecalibacterium prausnitzii abundance was significantly higher in individuals with HL and in those exhibiting greater resistance to amoxicillin. Conclusions: These findings provide preliminary evidence connecting the gut resistome with auditory function, supporting the emerging concept of a gut–ear–brain axis and underscoring the need for further research into microbiome-related mechanisms underlying HL. Full article