BACKGROUND: Age-related neurodegenerative diseases (NDs) pose a formidable challenge to healthcare systems worldwide due to their complex pathogenesis, significant morbidity, and mortality. Scope and Approach: This comprehensive review aims to elucidate the central role of the microbiotagut- brain axis (MGBA) in ND pathogenesis. Specifically, it delves into the perturbations within the gut microbiota and its metabolomic landscape, as well as the structural and functional transformations of the gastrointestinal and blood-brain barrier interfaces in ND patients. Additionally, it provides a comprehensive overview of the recent advancements in medicinal and dietary interventions tailored to modulate the MGBA for ND therapy. CONCLUSION: Accumulating evidence underscores the pivotal role of the gut microbiota in ND pathogenesis through the MGBA. Dysbiosis of the gut microbiota and associated metabolites instigate structural modifications and augmented permeability of both the gastrointestinal barrier and the blood-brain barrier (BBB). These alterations facilitate the transit of microbial molecules from the gut to the brain via neural, endocrine, and immune pathways, potentially contributing to the etiology of NDs. Numerous investigational strategies, encompassing prebiotic and probiotic interventions, pharmaceutical trials, and dietary adaptations, are actively explored to harness the microbiota for ND treatment. This work endeavors to enhance our comprehension of the intricate mechanisms underpinning ND pathogenesis, offering valuable insights for the development of innovative therapeutic modalities targeting these debilitating disorders.

• Klíčová slova
• Neurodegenerative diseases, blood-brain barrier, dietary adaptations., gut microbiota, microbiota-gut-brain axis, therapy,
• MeSH
• dysbióza metabolismus   MeSH
• hematoencefalická bariéra metabolismus   MeSH
• lidé MeSH
• mozek * metabolismus   MeSH
• neurodegenerativní nemoci * mikrobiologie   metabolismus   MeSH
• osa mozek-střevo * fyziologie   MeSH
• probiotika MeSH
• stárnutí * MeSH
• střevní mikroflóra * fyziologie   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH

Schizophrenia research arose in the twentieth century and is currently rapidly developing, focusing on many parallel research pathways and evaluating various concepts of disease etiology. Today, we have relatively good knowledge about the generation of positive and negative symptoms in patients with schizophrenia. However, the neural basis and pathophysiology of schizophrenia, especially cognitive symptoms, are still poorly understood. Finding new methods to uncover the physiological basis of the mental inabilities related to schizophrenia is an urgent task for modern neuroscience because of the lack of specific therapies for cognitive deficits in the disease. Researchers have begun investigating functional crosstalk between NMDARs and GABAergic neurons associated with schizophrenia at different resolutions. In another direction, the gut microbiota is getting increasing interest from neuroscientists. Recent findings have highlighted the role of a gut-brain axis, with the gut microbiota playing a crucial role in several psychopathologies, including schizophrenia and autism.There have also been investigations into potential therapies aimed at normalizing altered microbiota signaling to the enteric nervous system (ENS) and the central nervous system (CNS). Probiotics diets and fecal microbiota transplantation (FMT) are currently the most common therapies. Interestingly, in rodent models of binge feeding, optogenetic applications have been shown to affect gut colony sensitivity, thus increasing colonic transit. Here, we review recent findings on the gut microbiota-schizophrenia relationship using in vivo optogenetics. Moreover, we evaluate if manipulating actors in either the brain or the gut might improve potential treatment research. Such research and techniques will increase our knowledge of how the gut microbiota can manipulate GABA production, and therefore accompany changes in CNS GABAergic activity.

• Klíčová slova
• Fecal microbiota transplantation, Gut microbiota, Gut optogenetics, NMDA hypoactivity, NMDARs/GABA interaction, Probiotic dietaries, Schizophrenia,
• MeSH
• lidé MeSH
• mozek MeSH
• optogenetika MeSH
• osa mozek-střevo MeSH
• probiotika * MeSH
• schizofrenie * terapie   MeSH
• střevní mikroflóra * MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH

This review covers recent data on the relationship between major depressive disorder (MDD) and faecal microbiome and examines the co-relations between the use of probiotics and changes in psychiatric state. We conducted a thorough search of academic databases for articles published between 2018 and 2022, using specific keywords and previously established inclusion/exclusion criteria regarding faecal microbiota, depressive disorder, and probiotics. Of 192 eligible articles (reviews, original papers, and clinical trials), we selected 10 that fully met our criteria and performed a careful review to determine any correlation between microbiome, probiotic treatment, and depression. All patients were adults (mean age, 36.8), with at least one MDD episode and onset of depression during adolescence (duration of 31.39 years of depressive episodes). We found mixed but mostly positive results regarding the influence of probiotic/prebiotic/postbiotic effects on depression. We could not identify the precise mechanism of action that led to their improvement. Antidepressants did not alter the microbiota, according to studies that evaluated this aspect. Probiotic/prebiotic/postbiotic treatments were proven to be safe, with few and mild side effects. Probiotics seemingly could be beneficial in patients with depression, as evidenced by well-established depression scales. Based on this finding and the high tolerability and safety of probiotics, no caveats against their routine use can be made. Some unmet needs in this field include determination of the dominant type of microbiota in specific patients with depression; study of microbiome-directed/driven treatment regarding dose and duration adjustments; and multiple versus single strain treatments.

• Klíčová slova
• depression, depressive disorder, microbiota, probiotics,
• MeSH
• deprese etiologie   MeSH
• depresivní porucha unipolární * farmakoterapie   psychologie   MeSH
• dospělí MeSH
• lidé MeSH
• mikrobiota * MeSH
• mladiství MeSH
• osa mozek-střevo MeSH
• probiotika * terapeutické užití   farmakologie   MeSH
• Check Tag
• dospělí MeSH
• lidé MeSH
• mladiství MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH

Dietary restriction (DR) slows aging in many animals, while in some cases, the sensory signals from diet alone are sufficient to retard or accelerate lifespan. The digestive tract is a candidate location to sense nutrients, where neuropeptides secreted by enteroendocrine cells (EEC) produce systemic signals in response to food. Here, we measure how Drosophila neuropeptide F (NPF) is secreted into adult circulation by EEC and find that specific EEC differentially respond to dietary sugar and yeast. Female lifespan is increased when gut NPF is genetically depleted, and this manipulation is sufficient to blunt the longevity benefit conferred by DR. Depletion of NPF receptors at insulin-producing neurons of the brain also increases female lifespan, consistent with observations where loss of gut NPF decreases neuronal insulin secretion. The longevity conferred by repressing gut NPF and brain NPF receptors is reversed by treating adults with a juvenile hormone (JH) analog. JH is produced by the adult corpora allata, and inhibition of the insulin receptor at this tissue decreases JH titer and extends lifespan in both males and females, while this longevity is restored to wild type by treating adults with a JH analog. Overall, EEC of the gut modulate Drosophila aging through interorgan communication mediated by a gut-brain-corpora allata axis, and insulin produced in the brain impacts lifespan through its control of JH titer. These data suggest that we consider how human incretins and their analogs, which are used to treat obesity and diabetes, may impact aging.

• Klíčová slova
• aging, incretin, insulin, interorgan communication, juvenile hormone,
• MeSH
• dlouhověkost fyziologie   MeSH
• Drosophila melanogaster metabolismus   MeSH
• enteroendokrinní buňky metabolismus   MeSH
• inzulin * metabolismus   MeSH
• juvenilní hormony * metabolismus   MeSH
• mozek metabolismus   MeSH
• neurony metabolismus   MeSH
• neuropeptidy * metabolismus   MeSH
• osa mozek-střevo * fyziologie   MeSH
• proteiny Drosophily * metabolismus   genetika   MeSH
• stárnutí metabolismus   fyziologie   MeSH
• zvířata MeSH
• Check Tag
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• inzulin * MeSH
• juvenilní hormony * MeSH
• neuropeptide F, Drosophila MeSH Prohlížeč
• neuropeptidy * MeSH
• proteiny Drosophily * MeSH

There is increasing evidence of a pivotal role of the gut microbiota (GUT-M) in key physiological functions in vertebrates. Many studies discuss functional implications of the GUT-M not only on immunity, growth, metabolism, but also on brain development and behavior. However, while the influence of the microbiota-gut-brain axis (MGBA) on behavior is documented in rodents and humans, data on farm animals are scarce. This review will first report the well-known influence of the MGBA on behavior in rodent and human and then describe its influence on emotion, memory, social and feeding behaviors in farm animals. This corpus of experiments suggests that a better understanding of the effects of the MGBA on behavior could have large implications in various fields of animal production. Specifically, animal welfare and health could be improved by selection, nutrition and management processes that take into account the role of the GUT-M in behavior.

• Klíčová slova
• Behavior, Emotion, Livestock, Microbiota, Microbiota-gut-brain axis, Welfare,
• MeSH
• chování zvířat fyziologie   MeSH
• fyziologie výživy zvířat MeSH
• hospodářská zvířata fyziologie   MeSH
• lidé MeSH
• mozek fyziologie   MeSH
• pohoda zvířat * MeSH
• střevní mikroflóra fyziologie   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH

Anorexia nervosa is a psychiatric disorder defined by an extremely low body weight, a devastating fear of weight gain, and body image disturbance, however the etiopathogenesis remains unclear. The objective of the article is to provide a comprehensive review on the potential role of gut microbiota in pathogenesis of anorexia nervosa. Recent advances in sequencing techniques used for microbial detection revealed that this disease is associated with disruption of the composition of normal gut microbiota (dysbiosis), manifested by low microbial diversity and taxonomic differences as compared to healthy individuals. Microorganisms present in the gut represent a part of the so called "microbiota-gut-brain" axis that affect the central nervous system and thus human behavior via the production of various neuroactive compounds. In addition, cells of the immune system are equipped with receptors for these neuroactive substances. Microbiota of the intestinal system also represent a very important antigenic source. These antigens can mimic some host neuropeptides and neurohormones and thus trigger the production of autoantibodies which cross-react with these compounds. The levels and affinities of these antibodies are thought to be associated with neuropsychiatric conditions including anxiety, depression, and eating and sleep disorders. The study of microbiota function in diseases could bring new insights to the pathogenetic mechanisms.

• Klíčová slova
• Dysbiosis, Intestinal microbiome, Microbiota-gut-brain axis, Neuropeptide, Probiotics, Psychoneuroimmunology,
• MeSH
• lidé MeSH
• mentální anorexie imunologie   mikrobiologie   MeSH
• mozek imunologie   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH

The composition of microbiota and the gut-brain axis is increasingly considered a factor in the development of various pathological conditions. The etiology of multiple sclerosis (MS), a chronic autoimmune disease affecting the CNS, is complex and interactions within the gut-brain axis may be relevant in the development and the course of MS. In this article, we focus on the relationship between gut microbiota and the pathophysiology of MS. We review the contribution of germ-free mouse studies to our understanding of MS pathology and its implications for treatment strategies to modulate the microbiome in MS. This summary highlights the need for a better understanding of the role of the microbiota in patients' responses to disease-modifying drugs in MS and disease activity overall.

• Klíčová slova
• disease-modifying drugs, gut-brain axis, microbiome, multiple sclerosis,
• MeSH
• lidé MeSH
• mikrobiota * MeSH
• myši MeSH
• osa mozek-střevo MeSH
• roztroušená skleróza * MeSH
• střevní mikroflóra * MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH

It has become apparent that the molecular and biochemical integrity of interactive families, genera, and species of human gut microflora is critically linked to maintaining complex metabolic and behavioral processes mediated by peripheral organ systems and central nervous system neuronal groupings. Relatively recent studies have established intrinsic ratios of enterotypes contained within the human microbiome across demographic subpopulations and have empirically linked significant alterations in the expression of bacterial enterotypes with the initiation and persistence of several major metabolic and psychiatric disorders. Accordingly, the goal of our review is to highlight potential thematic/functional linkages of pathophysiological alterations in gut microbiota and bidirectional gut-brain signaling pathways with special emphasis on the potential roles of gut dysbiosis on the pathophysiology of psychiatric illnesses. We provide critical discussion of putative thematic linkages of Parkinson's disease (PD) data sets to similar pathophysiological events as potential causative factors in the development and persistence of diverse psychiatric illnesses. Finally, we include a concise review of preclinical paradigms that involve immunologically-induced GI deficits and dysbiosis of maternal microflora that are functionally linked to impaired neurodevelopmental processes leading to affective behavioral syndromes in the offspring.

• Klíčová slova
• Antibiotics, Bacteria, Depression, FOXG1, Microbiome, Monoamines, Psychiatry,
• MeSH
• duševní poruchy genetika   patofyziologie   MeSH
• dysbióza genetika   MeSH
• lidé MeSH
• mikrobiota genetika   MeSH
• mozek metabolismus   patofyziologie   MeSH
• Parkinsonova nemoc genetika   patofyziologie   MeSH
• střevní mikroflóra genetika   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH

Psychiatric and mood disorders may play an important role in the development and persistence of irritable bowel syndrome (IBS). Previously, we hypothesized that stress-induced implicit memories may persist throughout life via epigenetic processes in the enteric nervous system (ENS), independent of the central nervous system (CNS). These epigenetic memories in the ENS may contribute to developing and perpetuating IBS. Here, we further elaborate on our earlier hypothesis. That is, during pregnancy, maternal prenatal stresses perturb the HPA axis and increase circulating cortisol levels, which can affect the maternal gut microbiota. Maternal cortisol can cross the placental barrier and increase cortisol-circulating levels in the fetus. This leads to dysregulation of the HPA axis, affecting the gut microbiota, microbial metabolites, and intestinal permeability in the fetus. Microbial metabolites, such as short-chain fatty acids (which also regulate the development of fetal ENS), can modulate a range of diseases by inducing epigenetic changes. These mentioned processes suggest that stress-related, implicit, long-term epigenetic memories may be programmed into the fetal ENS during pregnancy. Subsequently, this implicit epigenetic stress information from the fetal ENS could be conveyed to the CNS through the bidirectional microbiota-gut-brain axis (MGBA), leading to perturbed functional connectivity among various brain networks and the dysregulation of affective and pain processes.

• Klíčová slova
• ENS, IBS, Implicit epigenetic long-term memory, Microbiota-gut-brain axis, short-chain fatty acids., stress,
• MeSH
• epigeneze genetická * MeSH
• lidé MeSH
• osa mozek-střevo fyziologie   MeSH
• psychický stres * metabolismus   MeSH
• střevní mikroflóra fyziologie   MeSH
• střevní nervový systém * MeSH
• syndrom dráždivého tračníku * metabolismus   MeSH
• těhotenství MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• těhotenství MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH

BACKGROUND: The brain-gut-microbiome (BGM) axis is a communication network through which the brain and gastrointestinal microbiota interact via neural, hormonal, immune, and gene expression mechanisms. Gut microbiota dysbiosis is thought to contribute to neurocognitive disorders, including perioperative neurocognitive disorder (PND), and to various metabolic abnormalities. Recently, we reported that sevoflurane induces neurocognitive deficits in exposed rats as well as their future offspring, with male offspring being particularly affected (intergenerational PND). In this study, we examined in the same animals whether the intergenerational effects of sevoflurane involve abnormalities in the BGM axis, and whether they are mitigated by paternal pretreatment with either the Na+-K+-Cl- (NKCC1) Cl- transporter inhibitor bumetanide or the glucocorticoid receptor inhibitor RU486, as previously demonstrated for neurocognitive deficits. METHODS: Male Sprague Dawley rats (F0 generation) were exposed to 2.1% sevoflurane for 3 hours on postnatal days 56, 58, and 60 (F0M_S group). Prior to each sevoflurane exposure, distinct experimental groups of F0 males received bumetanide (F0M_BS group) or RU486 (F0M_RS group). These males were mated on postnatal day 90 to produce offspring (F1 generation). Gut microbiota were profiled using 16S rRNA gene sequencing, and brain changes analyzed via RNA sequencing of hippocampal samples. RESULTS: F1 male offspring of F0M_S sires exhibited heightened corticosterone responses to stress, increased inflammatory markers, altered hippocampal transcriptomes, gut microbiota dysbiosis, elevated serum low-density lipoprotein cholesterol levels, and increased body weight. The only abnormality observed in F1 females was a shift in microbial diversity. F0M_S displayed profound alterations in hippocampal transcriptome, while microbial diversity was the only parameter affected in their gut microbiota. Bumetanide or RU486 mitigated most abnormalities, except increased body weight in F1 males. CONCLUSION: Paternal sevoflurane exposure in rats induces BGM axis abnormalities, particularly in male offspring, despite the absence of direct anesthetic exposure. Pretreatment with bumetanide or RU486 showed therapeutic efficacy.

• Publikační typ
• časopisecké články MeSH