Limited evidence for anatomical contacts between intestinal GLP-1 cells and vagal neurons in male mice.

The communication between intestinal Glucagon like peptide 1 (GLP-1)-producing cells and the peripheral nervous system has garnered renewed interest considering the availability of anti-obesity and anti-diabetic approaches targeting GLP-1 signaling. While it is well-established that intestinal GLP-1 cells can exert influence through paracrine mechanisms, recent evidence suggests the possible existence of synaptic-like connections between GLP-1 cells and peripheral neurons, including those of the vagus nerve. In this study, using a reporter Phox2b-Cre-Tomato mouse model and super-resolution confocal microscopy, we demonstrated that vagal axons made apparent contacts with less than 0.5% of GLP-1 cells. Moreover, immunohistochemistry combined with super-resolution confocal microscopy revealed abundant post-synaptic density 95 (PSD-95) immunoreactivity within the enteric plexus of the lower intestines of C57/BL6 mice, with virtually none in its mucosa. Lastly, utilizing RNAScope in situ hybridization in the lower intestines of mice, we observed that GLP-1 cells expressed generic markers of secretory cells such as Snap25 and Nefm, but neither synaptic markers such as Syn1 and Nrxn2, nor glutamatergic markers such as Slc17a7. Through theoretical considerations and a critical review of the literature, we concluded that intestinal GLP-1 cells primarily communicate with vagal neurons through paracrine mechanisms, rather than synaptic-like contacts.

Metagenomic symphony of the intestinal ecosystem: How the composition affects the mind.

Mental health disorders and neurodegenerative diseases place a heavy burden on patients and societies, and, although great strides have been made to understand the pathophysiology of these conditions, advancement in drug development is lagging. The importance of gastrointestinal health in maintaining overall health and preventing disease is not a new concept. Hundreds of years ago, healers from various cultures and civilizations recognized the crucial role of the gut in sustaining health. More than a century ago, scientists began exploring the restorative effects of probiotics, marking the early recognition of the importance of gut microbes. The omics era brought more enlightenment and enabled researchers to identify the complexity of the microbial ecosystems we harbour, encompassing bacteria, eukaryotes (including fungi), archaea, viruses, and other microorganisms. The extensive genetic capacity of the microbiota is dynamic and influenced by the environment. The microbiota therefore serves as a significant entity within us, with evolutionarily preserved functions in host metabolism, immunity, development, and behavior. The significant role of the bacterial gut microbiome in mental health and neurodegenerative disorders has been realized and described within the framework of the microbiota-gut-brain axis. However, the bacterial members do not function unaccompanied, but rather in concert, and there is a substantial knowledge gap regarding the involvement of non-bacterial microbiome members in these disorders. In this review, we will explore the current literature that implicates a role for the entire metagenomic ensemble, and how their complex interkingdom relationships could influence CNS functioning in mental health disorders and neurodegenerative diseases.

Innovative mechanisms of micro- and nanoplastic-induced brain injury: Emphasis on the microbiota-gut-brain axis.

Micro- and nanoplastics (MNPs), emerging environmental pollutants, infiltrate marine, terrestrial, and freshwater systems via diverse pathways, culminating in their accumulation in the human body through food chain transmission, posing potential health risks. Researches have demonstrated that MNPs disrupt gut microbiota equilibrium and compromise intestinal barrier integrity, as well as traverse the blood-brain barrier, leading to brain damage. Moreover, the complex interaction between the gut and the nervous system, facilitated by the "gut-brain axis," indicates an additional pathway for MNPs-induced brain damage. This has intensified scientific interest in the intercommunication between MNPs and the gut-brain axis. While existing studies have documented microbial imbalances and metabolic disruptions subsequent to MNPs exposure, the precise mechanisms by which the microbiota-gut-brain axis contributes to MNPs-induced central nervous system damage remain unclear. This review synthesizes current knowledge on the microbiota-gut-brain axis, elucidating the pathogenesis of MNPs-induced gut microbiota dysbiosis and its consequent brain injury. It emphasizes the complex interrelation between MNPs and the microbiota-gut-brain axis, advocating for the gut microbiota as a novel therapeutic target to alleviate MNP-induced brain harm.

Gut-Brain Axis and Neuroinflammation: The Role of Gut Permeability and the Kynurenine Pathway in Neurological Disorders.

The increasing prevalence of neurological disorders such as Alzheimer's, Parkinson's, and multiple sclerosis presents a significant global health challenge. Despite extensive research, the precise mechanisms underlying these conditions remain elusive, with current treatments primarily addressing symptoms rather than root causes. Emerging evidence suggests that gut permeability and the kynurenine pathway are involved in the pathogenesis of these neurological conditions, offering promising targets for novel therapeutic and preventive strategies. Gut permeability refers to the intestinal lining's ability to selectively allow essential nutrients into the bloodstream while blocking harmful substances. Various factors, including poor diet, stress, infections, and genetic predispositions, can compromise gut integrity, leading to increased permeability. This condition facilitates the translocation of toxins and bacteria into systemic circulation, triggering widespread inflammation that impacts neurological health via the gut-brain axis. The gut-brain axis (GBA) is a complex communication network between the gut and the central nervous system. Dysbiosis, an imbalance in the gut microbiota, can increase gut permeability and systemic inflammation, exacerbating neuroinflammation-a key factor in neurological disorders. The kynurenine pathway, the primary route for tryptophan metabolism, is significantly implicated in this process. Dysregulation of the kynurenine pathway in the context of inflammation leads to the production of neurotoxic metabolites, such as quinolinic acid, which contribute to neuronal damage and the progression of neurological disorders. This narrative review highlights the potential and progress in understanding these mechanisms. Interventions targeting the kynurenine pathway and maintaining a balanced gut microbiota through diet, probiotics, and lifestyle modifications show promise in reducing neuroinflammation and supporting brain health. In addition, pharmacological approaches aimed at modulating the kynurenine pathway directly, such as inhibitors of indoleamine 2,3-dioxygenase, offer potential avenues for new treatments. Understanding and targeting these interconnected pathways are crucial for developing effective strategies to prevent and manage neurological disorders.

Turicibacter and Catenibacterium as potential biomarkers in autism spectrum disorders.

Autism spectrum disorders (ASD) are neurodevelopmental disorders characterized by social, behavioral, and cognitive impairments. Several comorbidities, including gastrointestinal (GI) dysregulations, are frequently reported in ASD children. Although studies in animals have shown the crucial role of the microbiota in key aspects of neurodevelopment, there is currently no consensus on how the alteration of microbial composition affects the pathogenesis of ASD. Moreover, disruption of the gut-brain axis (GBA) has been reported in ASD although with limited studies conducted on the Mediterranean population. In our study, we aimed to investigate gut microbiota composition in Lebanese ASD subjects, their unaffected siblings, and a control group from various regions in Lebanon using the 16 S-rRNA sequencing (NGS). Our study revealed a lower abundance of Turicibacter and a significant enrichment on Proteobacteria in the ASD and siblings' groups compared to the controls, indicating that gut microbiota is probably affected by dietary habits, living conditions together with host genetic factors. The study also showed evidence of changes in the gut microbiome of ASD children compared to their siblings and the unrelated control. Bacteroidetes revealed a lower abundance in the ASD group compared to controls and siblings, conversely, Catenibacterium and Tenericutes revealed an increased abundance in the ASD group. Notably, our study identifies alterations in the abundance of Turicibacter and Catenibacterium in ASD children suggesting a possible link between these bacterial taxa and ASD and contributing to the growing body of evidence linking the microbiome to ASD.

Mini Review: The gut microbiota as a link between Alzheimer's disease and obesity.

Alzheimer's disease (AD) is a degenerative disease that causes a progressive decline in memory and thinking skills. Over the past few years, diverse studies have shown that there is no single cause of AD; instead, it has been reported that factors such as genetics, lifestyle, and environment contribute to the pathogenesis of the disease. In this sense, it has been shown that obesity during middle age is one of the most prominent modifiable risk factors for AD. Of the multiple potential mechanisms linking obesity and AD, the gut microbiota (GM) has gained increasing attention in recent years. However, the underlying mechanisms that connect the GM with the process of neurodegeneration remain unclear. Through this narrative review, we present a comprehensive understanding of how alterations in the GM of people with obesity may result in systemic inflammation and affect pathways related to the pathogenesis of AD. We conclude with an analysis of the relationship between the GM and insulin resistance, a risk factor for AD that is highly prevalent in people with obesity. Understanding the crosstalk between obesity, the GM, and the pathogenesis of AD will help to design new strategies aimed at preventing neurodegeneration.

Type 17 immunity: novel insights into intestinal homeostasis and autoimmune pathogenesis driven by gut-primed T cells.

The IL-23 signaling pathway in both innate and adaptive immune cells is vital for orchestrating type 17 immunity, which is marked by the secretion of signature cytokines such as IL-17, IL-22, and GM-CSF. These proinflammatory mediators play indispensable roles in maintaining intestinal immune equilibrium and mucosal host defense; however, their involvement has also been implicated in the pathogenesis of chronic inflammatory disorders, such as inflammatory bowel diseases and autoimmunity. However, the implications of type 17 immunity across diverse inflammation models are complex. This review provides a comprehensive overview of the multifaceted roles of these cytokines in maintaining gut homeostasis and in perturbing gut barrier integrity, leading to acute and chronic inflammation in various models of gut infection and colitis. Additionally, this review focuses on type 17 immunity interconnecting multiple organs in autoimmune conditions, with a particular emphasis on the pathogenesis of autoimmune arthritis and neuroinflammation driven by T cells primed within the gut microenvironment.

Adherence to the Mediterranean Diet: A Tool to the Therapeutic Approaches for Patients With Temporomandibular Joint Disorders.

BACKGROUND AND AIM: Temporomandibular joint disorder (TMD) is characterized by symptoms such as clenching, clicking, and locking of the jaw, often due to improper positioning affecting occlusion. Nearly half of TMD patients rarely require treatment, as symptoms typically diminish on their own within a year. Nevertheless, a significant majority of persons who are diagnosed with TMD do necessitate therapy, and it may take up to three years for complete remission to occur. This study aims to determine the extent to which a healthy nutritional model, specifically the Mediterranean diet, can enhance the effectiveness of existing therapeutic treatments, like physiotherapy with warm pads. METHODS: An interventional study design was implemented. Baseline scores were obtained pre- and post-intervention, while Mediterranean diet adherence was evaluated once at the beginning. A dependent samples t-test and a one-way multivariate analysis of covariance (MANCOVA) were used to test the experimental hypotheses. RESULTS: There is a statistically significant difference (p=0.04) between the three groups associated with Mediterranean diet adherence, as indicated by the mean differences on the Jaw Functional Limitation Scale (JFLS-20) questionnaire. Participants following a medium or high level of Mediterranean diet (≥18) reported fewer problems with jaw functionality both before and after the intervention compared to those with low (<18) adherence to the diet. CONCLUSION: Adherence to the Mediterranean diet appears to have a therapeutic effect on patients with TMD, offering a new dimension to their treatment. The primary benefit is the low cost of treatment, as the diet is easily accessible. This dietary approach could significantly enhance the management of TMD symptoms.

Therapeutic approaches targeting the gut microbiota in ischemic stroke: current advances and future directions.

Ischemic stroke (IS) is the predominant form of stroke pathology, and its clinical management remains constrained by therapeutic time frame. The gut microbiota (GM), comprising a multitude of bacterial and archaeal cells, surpasses the human cell count by approximately tenfold and significantly contributes to the human organism's growth, development, and overall well-being. The microbiota-gut-brain axis (MGBA) in recent years has established a strong association between gut microbes and the brain, demonstrating their intricate involvement in the progression of IS. The regulation of IS by the GM, encompassing changes in composition, abundance, and distribution, is multifaceted, involving neurological, endocrine, immunological, and metabolic mechanisms. This comprehensive understanding offers novel insights into the therapeutic approaches for IS. The objective of this paper is to examine the mechanisms of interaction between the GM and IS in recent years, assess the therapeutic effects of the GM on IS through various interventions, such as dietary modifications, probiotics, fecal microbiota transplantation, and antibiotics, and offer insights into the potential clinical application of the GM in stroke treatment.

Exploring the pathogenesis of insomnia and acupuncture intervention strategies based on the microbiota-gut-brain axis.

Insomnia is a common sleep disorder observed in clinical settings, with a globally rising prevalence rate. It not only impairs sleep quality and daytime functioning but also contributes to a range of physiological and psychological conditions, often co-occurring with somatic and mental disorders. Currently, the pathophysiology of this condition is not fully understood. Treatment primarily involves symptomatic management with benzodiazepine receptor agonists, melatonin and its receptor agonists, sedative antidepressants, atypical antipsychotics, and orexin receptor antagonists. However, due to the adverse side effects of these drugs, including dependency, addiction, and tolerance, there is an urgent need for safer, more effective, and environmentally friendly treatment methods. In recent years, research on the microbiota-gut-brain axis has received significant attention and is expected to be key in uncovering the pathogenesis of insomnia. Acupuncture stimulates acupoints, activating the body's intrinsic regulatory abilities and exerting multi-pathway, multi-target regulatory effects. A substantial body of evidence-based research indicates that acupuncture is effective in treating insomnia. However, the unclear mechanisms of its action have limited its further clinical application in insomnia treatment. Therefore, this study aims to elucidate the pathogenesis of insomnia from the perspective of the microbiota-gut-brain axis by examining metabolic, neuro-endocrine, autonomic nervous, and immune pathways. Additionally, this study discusses the comprehensive application of acupuncture in treating insomnia, aiming to provide new strategies for its treatment.

Regulation of hippocampal miRNA expression by intestinal flora in anxiety-like mice.

This study investigated the possible interaction between gut flora and miRNAs and the effect of both on anxiety disorders. The model group was induced with chronic restraint stress (CRS) and each group was tested for anxiety-like behaviour by open field test and elevated plus maze test. Meanwhile, the gut flora was analysed by 16S rRNA high-throughput sequencing. The miRNAs in hippocampus were analysed by high-throughput sequencing, and the key miRNAs were obtained by using the method of bioinformatics analysis. PCR was used to verify the significantly related key miRNAs. Spearman correlation analysis was used to explore the correlation between behaviour, key miRNAs and differential gut microbiota. The 16S rRNA high-throughput sequencing result showed that the gut flora was dysregulated in the model group. In particular, Verrucomicrobia, Akkermansia, Anaerostipes, Ralstonia, Burkholderia and Anaeroplasma were correlated with behaviour. The results of miRNA high-throughput sequencing analysis and bioinformatics analysis showed that 7 key miRNAs influenced the pathogenesis of anxiety, and qRT-PCR results were consistent with the high-throughput sequencing results. Mmu-miR-543-3p and mmu-miR-26a-5p were positively correlated with Verrucomicrobia, Akkermansia and Anaerostipes. Therefore, we infer that chronic stress caused the decrease of Akkermansia abundance, which may aggravate the decrease of mmu-miR-543-3p and mmu-miR-26a-5p expression, leading to the increase of SLC1A2 expression. In conclusion, gut flora has played an important influence on anxiety with changes in miRNAs.

Mechanistic insight of neurodegeneration due to micro/nano-plastic-induced gut dysbiosis.

Despite offering significant conveniences, plastic materials contribute substantially in developing environmental hazards and pollutants. Plastic trash that has not been adequately managed may eventually break down into fragments caused by human or ecological factors. Arguably, the crucial element for determining the biological toxicities of plastics are micro/nano-forms of plastics (MPs/NPs), which infiltrate the mammalian tissue through different media and routes. Infiltration of MPs/NPs across the intestinal barrier leads to microbial architectural dysfunction, which further modulates the population of gastrointestinal microbes. Thereby, it triggers inflammatory mediators (e.g., IL-1α/ß, TNF-α, and IFN-γ) by activating specific receptors located in the gut barrier. Mounting evidence indicates that MPs/NPs disrupt host pathophysiological function through modification of junctional proteins and effector cells. Moreover, the alteration of microbial diversity by MPs/NPs causes the breakdown of the blood-brain barrier and translocation of metabolites (e.g., SCFAs, LPS) through the vagus nerve. Potent penetration affects the neuronal networks, neuronal protein accumulation, acceleration of oxidative stress, and alteration of neurofibrillary tangles, and hinders distinctive communicating pathways. Conclusively, alterations of these neurotoxic factors are possibly responsible for the associated neurodegenerative disorders due to the exposure of MPs/NPs. In this review, the hypothesis on MPs/NPs associated with gut microbial dysbiosis has been interlinked to the distinct neurological impairment through the gut-brain axis.

Understanding neurotropic enteric viruses: routes of infection and mechanisms of attenuation.

The intricate connection between the gut and the brain involves multiple routes. Several viral families begin their infection cycle in the intestinal tract. However, amongst the long list of viral intestinal pathogens, picornaviruses, and astroviruses stand out for their ability to transition from the intestinal epithelia to central or peripheral nervous system cells. In immunocompromised, neonates and young children, these viral infections can manifest as severe diseases, such as encephalitis, meningitis, and acute flaccid paralysis. What confers this remarkable plasticity and makes them efficient in infecting cells of the gut and the brain axes? Here, we review the current understanding of the virus infection along the gut-brain axis for some enteric viruses and discuss the molecular mechanisms of their attenuation.

Gut microbiota metabolites: potential therapeutic targets for Alzheimer's disease?

Background: Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive decline in cognitive function, which significantly increases pain and social burden. However, few therapeutic interventions are effective in preventing or mitigating the progression of AD. An increasing number of recent studies support the hypothesis that the gut microbiome and its metabolites may be associated with upstream regulators of AD pathology. Methods: In this review, we comprehensively explore the potential mechanisms and currently available interventions targeting the microbiome for the improvement of AD. Our discussion is structured around modern research advancements in AD, the bidirectional communication between the gut and brain, the multi-target regulatory effects of microbial metabolites on AD, and therapeutic strategies aimed at modulating gut microbiota to manage AD. Results: The gut microbiota plays a crucial role in the pathogenesis of AD through continuous bidirectional communication via the microbiota-gut-brain axis. Among these, microbial metabolites such as lipids, amino acids, bile acids and neurotransmitters, especially sphingolipids and phospholipids, may serve as central components of the gut-brain axis, regulating AD-related pathogenic mechanisms including ß-amyloid metabolism, Tau protein phosphorylation, and neuroinflammation. Additionally, interventions such as probiotic administration, fecal microbiota transplantation, and antibiotic use have also provided evidence supporting the association between gut microbiota and AD. At the same time, we propose an innovative strategy for treating AD: a healthy lifestyle combined with targeted probiotics and other potential therapeutic interventions, aiming to restore intestinal ecology and microbiota balance. Conclusion: Despite previous efforts, the molecular mechanisms by which gut microbes act on AD have yet to be fully described. However, intestinal microorganisms may become an essential target for connecting the gut-brain axis and improving the symptoms of AD. At the same time, it requires joint exploration by multiple centers and multiple disciplines.

From gut to brain: unveiling probiotic effects through a neuroimaging perspective-A systematic review of randomized controlled trials.

The gut-brain axis, a bidirectional communication network between the gastrointestinal system and the brain, significantly influences mental health and behavior. Probiotics, live microorganisms conferring health benefits, have garnered attention for their potential to modulate this axis. However, their effects on brain function through gut microbiota modulation remain controversial. This systematic review examines the effects of probiotics on brain activity and functioning, focusing on randomized controlled trials using both resting-state and task-based functional magnetic resonance imaging (fMRI) methodologies. Studies investigating probiotic effects on brain activity in healthy individuals and clinical populations (i.e., major depressive disorder and irritable bowel syndrome) were identified. In healthy individuals, task-based fMRI studies indicated that probiotics modulate brain activity related to emotional regulation and cognitive processing, particularly in high-order areas such as the amygdala, precuneus, and orbitofrontal cortex. Resting-state fMRI studies revealed changes in connectivity patterns, such as increased activation in the Salience Network and reduced activity in the Default Mode Network. In clinical populations, task-based fMRI studies showed that probiotics could normalize brain function in patients with major depressive disorder and irritable bowel syndrome. Resting-state fMRI studies further suggested improved connectivity in mood-regulating networks, specifically in the subcallosal cortex, amygdala and hippocampus. Despite promising findings, methodological variability and limited sample sizes emphasize the need for rigorous, longitudinal research to clarify the beneficial effects of probiotics on the gut-brain axis and mental health.

Integrative microbiomics, proteomics and lipidomics studies unraveled the preventive mechanism of Shouhui Tongbian Capsules on cerebral ischemic stroke injury.

ETHNOPHARMACOLOGICAL RELEVANCE: Cerebral ischemic stroke (CIS) is one of the most important factors leading to death and disability, which seriously threaten the survival and health of patients. The intentional flora and its derived metabolites are demonstrated to play vital roles in the physiology and onset of CIS. Shouhui Tongbian Capsules (SHTB), a Traditional Chinese Medicine, could regulate gut microbiota and metabolites. Study has found that SHTB has protective effect on CIS, but the mechanism is still unclear. AIM OF STUDY: This study was designed to evaluate the preventive effects and the mechanism of SHTB on CIS injury. MATERIALS AND METHODS: The rats were pretreated with SHTB for 5 days, then the middle cerebral artery occlusion/reperfusion (MCAO/R) was established. Neurological deficit score, TTC staining, brain water content, H&E and Nissl staining were preformed to evaluate the preventive effects of SHTB on CIS. The Occludin and ZO-1 were analyzed to evaluate the blood-brain barrier (BBB). 16S rDNA sequencing and LC-ESI-MS/MS-based metabolomics profiling were performed to analyze the gut microbiota composition and short chain fatty acids (SCFAs) profile in gut. Serum lipopolysaccharide specific IgA antibody (LPS-SIgA) and diamine oxidase (DAO), as well as colon Claudin 5 and ZO-1 were analyzed to evaluate the intestinal barrier. Proteomics was used to evaluated the proteins profile in brain. Lipidomics were used to evaluate the brain SCFAs as well as medium and long chain fatty acids (MCFAs and LCFAs). Malondialdehyde (MDA), Total Superoxide dismutase (T-SOD), Glutathione (GSH), Glutathione peroxidase (GSH-Px), Catalase (CAT) and reactive oxygen species (ROS) were assayed to evaluate the oxidative stress in brain. Western blot was performed to evaluate the expression of PPARγ, Nrf2, SLC3A2, SCL7A11, GPX4, ACSL4 and LOX. RESULTS: SHTB prevented rats from MCAO/R injury, which was confirmed by lower cerebral infarct rate, brain water content, neurological deficit score and nissl body loss, and improved brain pathology. Meanwhile, SHTB upregulated the expression of ZO-1 and Occludin to maintain the integrity of BBB. 16S rDNA sequencing and LC-ESI-MS/MS-based targeted metabolomics found that SHTB increased the abundance of gut microbiota, regulated the numbers of intestinal bacteria to increase the production of Acetic acid, Propionic acid, and Butyric acid, as well as decrease the production of Valeric acid and Hexanoic acid in the gut. Meanwhile, SHTB improved the intestinal barrier by upregulating the protein levels of Claudin 5 and ZO-1, which was confirmed by low concentrations of LPS-SIgA and DAO in serum. Multi omics and spearman correlation analysis indicated that SHTB regulated the abundance of Escherichia-Shigella and Lactobacillus to increase Acetic acid, Propionic acid, and Butyric acid to induce the expression of PPARγ, thereby regulating fatty acid metabolism and degradation, improving lipid metabolism disorders, downregulating lipid oxidative stress, inhibiting ferroptosis, and alleviating brain injury. CONCLUSION: This study confirmed that SHTB improved the disturbance of fatty acid metabolism in brain tissue by regulating gut microbiota and the production of fecal SCFAs to inhibit ferroptosis caused by lipid oxidative stress and prevent CIS injury, which provided a potential candidate drug for the prevention of CIS.

Psychobiotic Properties of Lactiplantibacillus plantarum in Neurodegenerative Diseases.

Neurodegenerative disorders are the main cause of cognitive and physical disabilities, affect millions of people worldwide, and their incidence is on the rise. Emerging evidence pinpoints a disturbance of the communication of the gut-brain axis, and in particular to gut microbial dysbiosis, as one of the contributors to the pathogenesis of these diseases. In fact, dysbiosis has been associated with neuro-inflammatory processes, hyperactivation of the neuronal immune system, impaired cognitive functions, aging, depression, sleeping disorders, and anxiety. With the rapid advance in metagenomics, metabolomics, and big data analysis, together with a multidisciplinary approach, a new horizon has just emerged in the fields of translational neurodegenerative disease. In fact, recent studies focusing on taxonomic profiling and leaky gut in the pathogenesis of neurodegenerative disorders are not only shedding light on an overlooked field but are also creating opportunities for biomarker discovery and development of new therapeutic and adjuvant strategies to treat these disorders. Lactiplantibacillus plantarum (LBP) strains are emerging as promising psychobiotics for the treatment of these diseases. In fact, LBP strains are able to promote eubiosis, increase the enrichment of bacteria producing beneficial metabolites such as short-chain fatty acids, boost the production of neurotransmitters, and support the homeostasis of the gut-brain axis. In this review, we summarize the current knowledge on the role of the gut microbiota in the pathogenesis of neurodegenerative disorders with a particular focus on the benefits of LBP strains in Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, autism, anxiety, and depression.

The Latest Data Concerning the Etiology and Pathogenesis of Irritable Bowel Syndrome.

Globally, irritable bowel syndrome (IBS) is present in approximately 10% of the population. While this condition does not pose a risk of complications, it has a substantial impact on the patient's quality of life. Moreover, this disease has a significant financial impact on healthcare systems. This includes the direct costs associated with the diagnosis and treatment of these patients, as well as the indirect costs that arise from work absenteeism and reduced productivity. In light of these data, recent research has focused on elucidating the pathophysiological basis of this condition in order to improve the quality of life for affected individuals. Despite extensive research to date, we still do not fully understand the precise mechanisms underlying IBS. Numerous studies have demonstrated the involvement of the gut-brain axis, visceral hypersensitivity, gastrointestinal dysmotility, gut microbiota dysbiosis, food allergies and intolerances, low-grade mucosal inflammation, genetic factors, and psychosocial factors. The acquisition of new data is crucial for the advancement of optimal therapeutic approaches aimed at enhancing the general health of these patients while simultaneously reducing the financial burden associated with this ailment.

Okinawa-Based Nordic Diet Decreases Plasma Glial Fibrillary Acidic Protein Levels in Type 2 Diabetes Patients.

Elevated levels of glial fibrillary acidic protein (GFAP) in plasma reflect neuroinflammation and are linked to cognitive decline. Preclinical studies show that dietary change can attenuate astrocyte reactivity and neuroinflammation. In the current study, we investigate if the Okinawa-based Nordic (O-BN) diet alters plasma GFAP levels in patients with Type 2 Diabetes (T2D), a metabolic disorder associated with cognitive disturbances and an increased risk of dementia. Plasma GFAP levels were measured in T2D patients (n = 30) at baseline, after 3 months of the diet, and after a subsequent 4 months of unrestricted diets. The GFAP levels decreased significantly after 3 months of the diet (p = 0.048) but reverted to baseline levels after 4 months of unrestricted diets. At baseline, the GFAP levels correlated significantly with levels of the neurodegeneration marker neurofilament light polypeptide (r = 0.400*) and, after correcting for age, sex, and body mass index, with proinflammatory plasma cytokines (ranging from r = 0.440* to r = 0.530**) and the metabolic hormone islet amyloid polypeptide (r = 0.478*). We found no correlation with psychological well-being. These results suggest that the O-BN diet reduces neuroinflammation in T2D patients and may thus be an important preventive measure for managing T2D and reducing the risk of neurodegenerative disorders.