Journal articles on the topic 'Microbiota, gut-brain axis, epilepsy, inflammation'
To see the other types of publications on this topic, follow the link: Microbiota, gut-brain axis, epilepsy, inflammation.
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 50 journal articles for your research on the topic 'Microbiota, gut-brain axis, epilepsy, inflammation.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.
1
Lin, Yixin. "The Role of Ketogenic Diet in Gut Microbiota." Highlights in Science, Engineering and Technology 19 (November 17, 2022): 36–43. http://dx.doi.org/10.54097/hset.v19i.2692.
Full textAbstract:
Several studies point to a vital role for gut microbiota (GM) in preventing disease and reducing inflammation in humans. Gut microbiota has an important relationship with the human brain-gut axis, and the biological metabolites they produce are closely linked to the function of nervous system. Ketogenic diet (KD) is thought to be effective on the makeup of GM and thus affecting human health due to its low calorie and fiber consumption. Recent research has found KD can affect GM composition under pathological conditions, such as drug refractory epilepsy (DRE). So as to achieve the purpose of treating DRE. Therefore, this article aims to explore the effect of KD on the human GM and explore whether it has important implications for human health. Finally, we found that KD can modulate human health by affecting gut microbiota richness, increasing some microbes that can produce beneficial metabolites, and reducing some pro-inflammatory microbes to prevent and treat specific diseases.
2
Kharchenko, Yu V., H. I. Titov, D. H. Kryzhanovskyi, M. P. Fedchenko, H. P. Chernenko, V. V. Filipenko, and V. A. Miakushko. "Stress and the Gut-Brain Axis." Ukraïnsʹkij žurnal medicini, bìologìï ta sportu 7, no. 4 (August 30, 2022): 137–46. http://dx.doi.org/10.26693/jmbs07.04.137.
Full textAbstract:
The purpose of the review was to study the effects of stress on the gut microbiota. Results and discussion. The gut microbiota forms a complex microbial community that has a significant impact on human health. The composition of the microbiota varies from person to person, and it changes throughout life. It is known that the microbiome can be altered due to diet, various processes, such as inflammation and/or stress. Like all other areas of medicine, microbiology is constantly growing. The gut microbiota lives in a symbiotic relationship with the human host. It is now believed to interact with almost all human organs, including the central nervous system, in the so-called «gut-brain-microbiome axis». Recently, a growing level of research is showing that microbes play a much bigger role in our lives than previously thought, and can have a myriad of effects on how we behave and think, and even on our mental health. The relationship between the brain and the microbiota is bidirectional and includes endocrine, neuronal, immune, and metabolic pathways. The microbiota interacts with the brain through various mechanisms and mediators, including cytokines, short-chain fatty acids, hormones, and neurotransmitters. According to the hypothalamic-pituitary-adrenocortical axis imbalance theory, hormonal imbalances are closely related to psychiatric illness, anxiety, and stress disorders. Therefore, the gut microbiome is closely related to the development and functioning of this axis. The microbiota can influence neurotransmitter levels in a variety of ways, including the secretion of gamma-aminobutyric acid, norepinephrine, dopamine, and serotonin, and can even regulate serotonin synthesis. These neurotransmitters can influence the hormonal status of the body, and the hormones themselves can influence the formation of the qualitative and quantitative composition of the microbiota. Accordingly, a change in the composition of the intestinal microbiota may be responsible for modifying the hormonal levels of the human body. The endocrine environment in the gut can also be modulated through the neuro-enteroendocrine system. Conclusion. Today, it is known that microbiota changes can be associated with several disorders of the nervous system, such as neuropsychiatric, neurodegenerative and neuroinflammatory processes. Research in recent decades has shown that disorders of the nervous system and mood disorders are associated with changes in the balance of neurotransmitters in the brain. Therefore, understanding the role of microbiota in the development and functioning of the brain is of great importance
3
Dumitrescu, Laura, Iulia Popescu-Olaru, Liviu Cozma, Delia Tulbă, Mihail Eugen Hinescu, Laura Cristina Ceafalan, Mihaela Gherghiceanu, and Bogdan Ovidiu Popescu. "Oxidative Stress and the Microbiota-Gut-Brain Axis." Oxidative Medicine and Cellular Longevity 2018 (December 9, 2018): 1–12. http://dx.doi.org/10.1155/2018/2406594.
Full textAbstract:
The gut-brain axis is increasingly recognized as an important pathway of communication and of physiological regulation, and gut microbiota seems to play a significant role in this mutual relationship. Oxidative stress is one of the most important pathogenic mechanisms for both neurodegenerative diseases, such as Alzheimer’s or Parkinson’s, and acute conditions, such as stroke or traumatic brain injury. A peculiar microbiota type might increase brain inflammation and reactive oxygen species levels and might favor abnormal aggregation of proteins. Reversely, brain lesions of various etiologies result in alteration of gut properties and microbiota. These recent hypotheses could open a door for new therapeutic approaches in various neurological diseases.
4
Gernone, Floriana, Annamaria Uva, Marco Silvestrino, Maria Alfonsa Cavalera, and Andrea Zatelli. "Role of Gut Microbiota through Gut–Brain Axis in Epileptogenesis: A Systematic Review of Human and Veterinary Medicine." Biology 11, no. 9 (August 30, 2022): 1290. http://dx.doi.org/10.3390/biology11091290.
Full textAbstract:
Canine idiopathic epilepsy is a common neurological disease characterized by the enduring predisposition of the cerebral cortex to generate seizures. An etiological explanation has not been fully identified in humans and dogs, and, among the presumed causes, several studies support the possible involvement of gut microbiota. In this review, the authors summarize the evidence of the reasonable role of gut microbiota in epilepsy through the so-called gut–brain axis. The authors provide an overview of recent clinical and preclinical studies in humans and dogs in which the modulation of intestinal permeability, the alteration of local immune response, and the alteration in production of essential metabolites and neurotransmitters associated with dysbiosis could be responsible for the pathogenesis of canine epilepsy. A systematic review of the literature, following the PRISMA guidelines, was performed in two databases (PubMed and Web of Science). Eleven studies were included and reviewed supporting the connection between gut microbiota and epilepsy via the gut–brain axis.
5
Barber, Thomas M., Georgios Valsamakis, George Mastorakos, Petra Hanson, Ioannis Kyrou, Harpal S. Randeva, and Martin O. Weickert. "Dietary Influences on the Microbiota–Gut–Brain Axis." International Journal of Molecular Sciences 22, no. 7 (March 28, 2021): 3502. http://dx.doi.org/10.3390/ijms22073502.
Full textAbstract:
Over unimaginable expanses of evolutionary time, our gut microbiota have co-evolved with us, creating a symbiotic relationship in which each is utterly dependent upon the other. Far from confined to the recesses of the alimentary tract, our gut microbiota engage in complex and bi-directional communication with their host, which have far-reaching implications for overall health, wellbeing and normal physiological functioning. Amongst such communication streams, the microbiota–gut–brain axis predominates. Numerous complex mechanisms involve direct effects of the microbiota, or indirect effects through the release and absorption of the metabolic by-products of the gut microbiota. Proposed mechanisms implicate mitochondrial function, the hypothalamus–pituitary–adrenal axis, and autonomic, neuro-humeral, entero-endocrine and immunomodulatory pathways. Furthermore, dietary composition influences the relative abundance of gut microbiota species. Recent human-based data reveal that dietary effects on the gut microbiota can occur rapidly, and that our gut microbiota reflect our diet at any given time, although much inter-individual variation pertains. Although most studies on the effects of dietary macronutrients on the gut microbiota report on associations with relative changes in the abundance of particular species of bacteria, in broad terms, our modern-day animal-based Westernized diets are relatively high in fats and proteins and impoverished in fibres. This creates a perfect storm within the gut in which dysbiosis promotes localized inflammation, enhanced gut wall permeability, increased production of lipopolysaccharides, chronic endotoxemia and a resultant low-grade systemic inflammatory milieu, a harbinger of metabolic dysfunction and many modern-day chronic illnesses. Research should further focus on the colony effects of the gut microbiota on health and wellbeing, and dysbiotic effects on pathogenic pathways. Finally, we should revise our view of the gut microbiota from that of a seething mass of microbes to one of organ-status, on which our health and wellbeing utterly depends. Future guidelines on lifestyle strategies for wellbeing should integrate advice on the optimal establishment and maintenance of a healthy gut microbiota through dietary and other means. Although we are what we eat, perhaps more importantly, we are what our gut microbiota thrive on and they thrive on what we eat.
6
Amlerova, Jana, Jan Šroubek, Francesco Angelucci, and Jakub Hort. "Evidences for a Role of Gut Microbiota in Pathogenesis and Management of Epilepsy." International Journal of Molecular Sciences 22, no. 11 (May 25, 2021): 5576. http://dx.doi.org/10.3390/ijms22115576.
Full textAbstract:
Epilepsy as a chronic neurological disorder is characterized by recurrent, unprovoked epileptic seizures. In about half of the people who suffer from epilepsy, the root cause of the disorder is unknown. In the other cases, different factors can cause the onset of epilepsy. In recent years, the role of gut microbiota has been recognized in many neurological disorders, including epilepsy. These data are based on studies of the gut microbiota–brain axis, a relationship starting by a dysbiosis followed by an alteration of brain functions. Interestingly, epileptic patients may show signs of dysbiosis, therefore the normalization of the gut microbiota may lead to improvement of epilepsy and to greater efficacy of anticonvulsant drugs. In this descriptive review, we analyze the evidences for the role of gut microbiota in epilepsy and hypothesize a mechanism of action of these microorganisms in the pathogenesis and treatment of the disease. Human studies revealed an increased prevalence of Firmicutes in patients with refractory epilepsy. Exposure to various compounds can change microbiota composition, decreasing or exacerbating epileptic seizures. These include antibiotics, epileptic drugs, probiotics and ketogenic diet. Finally, we hypothesize that physical activity may play a role in epilepsy through the modulation of the gut microbiota.
7
Sulistyo, Rikky Dwiyanto. "The Gut Microbiota in Epilepsy: Current Concepts of Mechanisms and Potential Therapeutics." European Journal of Biology and Biotechnology 3, no. 1 (February 8, 2022): 5–9. http://dx.doi.org/10.24018/ejbio.2022.3.1.331.
Full textAbstract:
Epilepsy is a non-communicable brain disorder characterized by an individual's proclivity for spontaneous epileptic seizures. Epilepsy may be classified into six types: genetic, structural, metabolic, infectious, immune-related, and unexplained causes. Numerous current findings have shown evidence that an imbalance in the gut microbiota is a cause of epilepsy. Between the gut microbiota and the brain systems, there are five putative communication pathways. The neuroendocrine hypothalamic-pituitary-adrenal (HPA) axis, intestinal bacteria's production of neurotransmitters, the intestinal immune system, and the relationship between the intestinal mucosal barrier and the blood-brain barrier are among them. Future epilepsy interventions might include modifications of antiepileptic medications, a ketogenic diet, and probiotics as a possible treatment in the gut flora. However, further research is required to assess long-term therapeutic benefits.
8
Gupta, Haripriya, Ki Tae Suk, and Dong Joon Kim. "Gut Microbiota at the Intersection of Alcohol, Brain, and the Liver." Journal of Clinical Medicine 10, no. 3 (February 2, 2021): 541. http://dx.doi.org/10.3390/jcm10030541.
Full textAbstract:
Over the last decade, increased research into the cognizance of the gut–liver–brain axis in medicine has yielded powerful evidence suggesting a strong association between alcoholic liver diseases (ALD) and the brain, including hepatic encephalopathy or other similar brain disorders. In the gut–brain axis, chronic, alcohol-drinking-induced, low-grade systemic inflammation is suggested to be the main pathophysiology of cognitive dysfunctions in patients with ALD. However, the role of gut microbiota and its metabolites have remained unclear. Eubiosis of the gut microbiome is crucial as dysbiosis between autochthonous bacteria and pathobionts leads to intestinal insult, liver injury, and neuroinflammation. Restoring dysbiosis using modulating factors such as alcohol abstinence, promoting commensal bacterial abundance, maintaining short-chain fatty acids in the gut, or vagus nerve stimulation could be beneficial in alleviating disease progression. In this review, we summarize the pathogenic mechanisms linked with the gut–liver–brain axis in the development and progression of brain disorders associated with ALD in both experimental models and humans. Further, we discuss the therapeutic potential and future research directions as they relate to the gut–liver–brain axis.
9
Sheng, Kangliang, Jian Yang, Yifan Xu, Xiaowei Kong, Jingmin Wang, and Yongzhong Wang. "Alleviation effects of grape seed proanthocyanidin extract on inflammation and oxidative stress in a d-galactose-induced aging mouse model by modulating the gut microbiota." Food & Function 13, no. 3 (2022): 1348–59. http://dx.doi.org/10.1039/d1fo03396d.
Full text
10
Xu, Hao-Ming, Hong-Li Huang, You-Lian Zhou, Hai-Lan Zhao, Jing Xu, Di-Wen Shou, Yan-Di Liu, Yong-Jian Zhou, and Yu-Qiang Nie. "Fecal Microbiota Transplantation: A New Therapeutic Attempt from the Gut to the Brain." Gastroenterology Research and Practice 2021 (January 16, 2021): 1–20. http://dx.doi.org/10.1155/2021/6699268.
Full textAbstract:
Gut dysbacteriosis is closely related to various intestinal and extraintestinal diseases. Fecal microbiota transplantation (FMT) is a biological therapy that entails transferring the gut microbiota from healthy individuals to patients in order to reconstruct the intestinal microflora in the latter. It has been proved to be an effective treatment for recurrent Clostridium difficile infection. Studies show that the gut microbiota plays an important role in the pathophysiology of neurological and psychiatric disorders through the microbiota-gut-brain axis. Therefore, reconstruction of the healthy gut microbiota is a promising new strategy for treating cerebral diseases. We have reviewed the latest research on the role of gut microbiota in different nervous system diseases as well as FMT in the context of its application in neurological, psychiatric, and other nervous system-related diseases (Parkinson’s disease, Alzheimer’s disease, multiple sclerosis, epilepsy, autism spectrum disorder, bipolar disorder, hepatic encephalopathy, neuropathic pain, etc.).
11
Leblhuber, Friedrich, Daniela Ehrlich, Kostja Steiner, Simon Geisler, Dietmar Fuchs, Lukas Lanser, and Katharina Kurz. "The Immunopathogenesis of Alzheimer’s Disease Is Related to the Composition of Gut Microbiota." Nutrients 13, no. 2 (January 25, 2021): 361. http://dx.doi.org/10.3390/nu13020361.
Full textAbstract:
The microbiota–gut–brain axis plays an important role in the development of neurodegenerative diseases. Commensal and pathogenic enteric bacteria can influence brain and immune system function by the production of lipopolysaccharides and amyloid. Dysbiosis of the intestinal microbiome induces local and consecutively systemic immune-mediated inflammation. Proinflammatory cytokines then trigger neuroinflammation and finally neurodegeneration. Immune-mediated oxidative stress can lead to a deficiency of vitamins and essential micronutrients. Furthermore, the wrong composition of gut microbiota might impair the intake and metabolization of nutrients. In patients with Alzheimer’s disease (AD) significant alterations of the gut microbiota have been demonstrated. Standard Western diet, infections, decreased physical activity and chronic stress impact the composition and diversity of gut microbiota. A higher abundancy of “pro-inflammatory” gut microbiota goes along with enhanced systemic inflammation and neuroinflammatory processes. Thus, AD beginning in the gut is closely related to the imbalance of gut microbiota. Modulation of gut microbiota by Mediterranean diet, probiotics and curcumin can slow down cognitive decline and alter the gut microbiome significantly. A multi-domain intervention approach addressing underlying causes of AD (inflammation, infections, metabolic alterations like insulin resistance and nutrient deficiency, stress) appears very promising to reduce or even reverse cognitive decline by exerting positive effects on the gut microbiota.
12
Chen, Keyin, Yuchen Wei, and Tianhao Xing. "The Gut Microbiota Dysbiosis as a Trigger of Inflammation-Driving Pathogensis of Alzheimer’s Disease." Highlights in Science, Engineering and Technology 8 (August 17, 2022): 306–13. http://dx.doi.org/10.54097/hset.v8i.1169.
Full textAbstract:
Alzheimer's disease (AD) is a degenerative disease of the central nervous system, and its pathogenesis is very complex. Gut microbiota is an immense and complicated microbial community that is regarded as the “second brain “by scientists. These microorganisms exist in the ecosystem of the gastrointestinal tract which is in the human body and form a relatively stable environment within the gastrointestinal tract. As a large number of microorganisms that can survive and coexist harmoniously in the human body, intestinal flora is a very important environmental factor and plays a very important role in the mutual transformation of people's health and diseases. On this basis, the cerebral intestinal axis is a two-way information regulation system that connects the brain and gastrointestinal functions. This means that intestinal microorganisms can participate in the brain-intestinal axis. Recent studies have shown that disturbances (compositional changes and translocations) of the gut microbiota are associated with neurological disorders (AD), where the gastrointestinal tract communicates with the central nervous system via the gut-brain axis, including direct effects on nerves, endocrine pathways, and immune regulation. Animal models, fecal microbiota transplantation, and probiotic interventions provide evidence for the association of gut microbiota with AD. The leaked bacterial metabolites may directly damage neuronal function, and may also induce neuroinflammation and promote the pathogenesis of AD. Therefore, the main goal of this review is to summarize, study and discuss the nowadays research and results of intestinal microbiota in Alzheimer-related mechanisms and to understand the relevance, function, and impact between the mechanism and Alzheimer’s disease.
13
Russo, Roberto, Claudia Cristiano, Carmen Avagliano, Carmen De Caro, Giovanna La Rana, Giuseppina Mattace Raso, Roberto Berni Canani, Rosaria Meli, and Antonio Calignano. "Gut-brain Axis: Role of Lipids in the Regulation of Inflammation, Pain and CNS Diseases." Current Medicinal Chemistry 25, no. 32 (October 16, 2018): 3930–52. http://dx.doi.org/10.2174/0929867324666170216113756.
Full textAbstract:
The human gut is a composite anaerobic environment with a large, diverse and dynamic enteric microbiota, represented by more than 100 trillion microorganisms, including at least 1000 distinct species. The discovery that a different microbial composition can influence behavior and cognition, and in turn the nervous system can indirectly influence enteric microbiota composition, has significantly contributed to establish the well-accepted concept of gut-brain axis. This hypothesis is supported by several evidence showing mutual mechanisms, which involve the vague nerve, the immune system, the hypothalamic-pituitaryadrenal (HPA) axis modulation and the bacteria-derived metabolites. Many studies have focused on delineating a role for this axis in health and disease, ranging from stress-related disorders such as depression, anxiety and irritable bowel syndrome (IBS) to neurodevelopmental disorders, such as autism, and to neurodegenerative diseases, such as Parkinson Disease, Alzheimer’s Disease etc. Based on this background, and considering the relevance of alteration of the symbiotic state between host and microbiota, this review focuses on the role and the involvement of bioactive lipids, such as the N-acylethanolamine (NAE) family whose main members are N-arachidonoylethanolamine (AEA), palmitoylethanolamide (PEA) and oleoilethanolamide (OEA), and short chain fatty acids (SCFAs), such as butyrate, belonging to a large group of bioactive lipids able to modulate peripheral and central pathologic processes. Their effective role has been studied in inflammation, acute and chronic pain, obesity and central nervous system diseases. A possible correlation has been shown between these lipids and gut microbiota through different mechanisms. Indeed, systemic administration of specific bacteria can reduce abdominal pain through the involvement of cannabinoid receptor 1 in the rat; on the other hand, PEA reduces inflammation markers in a murine model of inflammatory bowel disease (IBD), and butyrate, producted by gut microbiota, is effective in reducing inflammation and pain in irritable bowel syndrome and IBD animal models. In this review, we underline the relationship among inflammation, pain, microbiota and the different lipids, focusing on a possible involvement of NAEs and SCFAs in the gut-brain axis and their role in the central nervous system diseases.
14
Salvo, Eloisa, Patricia Stokes, Ciara E. Keogh, Ingrid Brust-Mascher, Carly Hennessey, Trina A. Knotts, Jessica A. Sladek, et al. "A murine model of pediatric inflammatory bowel disease causes microbiota-gut-brain axis deficits in adulthood." American Journal of Physiology-Gastrointestinal and Liver Physiology 319, no. 3 (September 1, 2020): G361—G374. http://dx.doi.org/10.1152/ajpgi.00177.2020.
Full textAbstract:
Here we describe long-lasting impacts on the microbiota-gut-brain (MGB) axis following administration of low-dose dextran sodium sulfate (DSS) to weaning mice (P21), including gut dysbiosis, colonic inflammation, and brain/behavioral deficits in adulthood (P56). Early-life DSS leads to acute colonic inflammation, similar to adult mice; however, it results in long-lasting deficits in the MGB axis in adulthood (P56), in contrast to the transient deficits seen in adult DSS. This model highlights the unique features of pediatric inflammatory bowel disease.
15
Oligschlaeger, Yvonne, Tulasi Yadati, Tom Houben, Claudia Maria Condello Oliván, and Ronit Shiri-Sverdlov. "Inflammatory Bowel Disease: A Stressed “Gut/Feeling”." Cells 8, no. 7 (June 30, 2019): 659. http://dx.doi.org/10.3390/cells8070659.
Full textAbstract:
Inflammatory bowel disease (IBD) is a chronic and relapsing intestinal inflammatory condition, hallmarked by a disturbance in the bidirectional interaction between gut and brain. In general, the gut/brain axis involves direct and/or indirect communication via the central and enteric nervous system, host innate immune system, and particularly the gut microbiota. This complex interaction implies that IBD is a complex multifactorial disease. There is increasing evidence that stress adversely affects the gut/microbiota/brain axis by altering intestinal mucosa permeability and cytokine secretion, thereby influencing the relapse risk and disease severity of IBD. Given the recurrent nature, therapeutic strategies particularly aim at achieving and maintaining remission of the disease. Alternatively, these strategies focus on preventing permanent bowel damage and concomitant long-term complications. In this review, we discuss the gut/microbiota/brain interplay with respect to chronic inflammation of the gastrointestinal tract and particularly shed light on the role of stress. Hence, we evaluated the therapeutic impact of stress management in IBD.
16
Zhou, Yingyu, Wanyi Qiu, Yimei Wang, Rong Wang, Tomohiro Takano, Xuyang Li, Zhangliang Zhu, et al. "β-Elemene Suppresses Obesity-Induced Imbalance in the Microbiota-Gut-Brain Axis." Biomedicines 9, no. 7 (June 22, 2021): 704. http://dx.doi.org/10.3390/biomedicines9070704.
Full textAbstract:
As a kind of metabolically triggered inflammation, obesity influences the interplay between the central nervous system and the enteral environment. The present study showed that β-elemene, which is contained in various plant substances, had effects on recovering the changes in metabolites occurring in high-fat diet (HFD)-induced obese C57BL/6 male mice brains, especially in the prefrontal cortex (PFC) and hippocampus (HIP). β-elemene also partially reversed HFD-induced changes in the composition and contents of mouse gut bacteria. Furthermore, we evaluated the interaction between cerebral metabolites and intestinal microbiota via Pearson correlations. The prediction results suggested that Firmicutes were possibly controlled by neuron integrity, cerebral inflammation, and neurotransmitters, and Bacteroidetes in mouse intestines might be related to cerebral aerobic respiration and the glucose cycle. Such results also implied that Actinobacteria probably affected cerebral energy metabolism. These findings suggested that β-elemene has regulatory effects on the imbalanced microbiota-gut-brain axis caused by obesity and, therefore, would contribute to the future study in on the interplay between cerebral metabolites from different brain regions and the intestinal microbiota of mice.
17
Ibrahim, Iddrisu, Soumyakrishnan Syamala, Joseph Atia Ayariga, Junhuan Xu, Boakai K. Robertson, Sreepriya Meenakshisundaram, and Olufemi S. Ajayi. "Modulatory Effect of Gut Microbiota on the Gut-Brain, Gut-Bone Axes, and the Impact of Cannabinoids." Metabolites 12, no. 12 (December 10, 2022): 1247. http://dx.doi.org/10.3390/metabo12121247.
Full textAbstract:
The gut microbiome is a collection of microorganisms and parasites in the gastrointestinal tract. Many factors can affect this community’s composition, such as age, sex, diet, medications, and environmental triggers. The relationship between the human host and the gut microbiota is crucial for the organism’s survival and development, whereas the disruption of this relationship can lead to various inflammatory diseases. Cannabidiol (CBD) and tetrahydrocannabinol (THC) are used to treat muscle spasticity associated with multiple sclerosis. It is now clear that these compounds also benefit patients with neuroinflammation. CBD and THC are used in the treatment of inflammation. The gut is a significant source of nutrients, including vitamins B and K, which are gut microbiota products. While these vitamins play a crucial role in brain and bone development and function, the influence of gut microbiota on the gut-brain and gut-bone axes extends further and continues to receive increasing scientific scrutiny. The gut microbiota has been demonstrated to be vital for optimal brain functions and stress suppression. Additionally, several studies have revealed the role of gut microbiota in developing and maintaining skeletal integrity and bone mineral density. It can also influence the development and maintenance of bone matrix. The presence of the gut microbiota can influence the actions of specific T regulatory cells, which can lead to the development of bone formation and proliferation. In addition, its metabolites can prevent bone loss. The gut microbiota can help maintain the bone’s equilibrium and prevent the development of metabolic diseases, such as osteoporosis. In this review, the dual functions gut microbiota plays in regulating the gut-bone axis and gut-brain axis and the impact of CBD on these roles are discussed.
18
Serra, Diana, Leonor M. Almeida, and Teresa C. P. Dinis. "The Impact of Chronic Intestinal Inflammation on Brain Disorders: the Microbiota-Gut-Brain Axis." Molecular Neurobiology 56, no. 10 (April 3, 2019): 6941–51. http://dx.doi.org/10.1007/s12035-019-1572-8.
Full text
19
Guo, Tong-Tong, Zheng Zhang, Yan Sun, Rui-Yang Zhu, Fei-Xia Wang, Lian-Ju Ma, Lin Jiang, and Han-Deng Liu. "Neuroprotective Effects of Sodium Butyrate by Restoring Gut Microbiota and Inhibiting TLR4 Signaling in Mice with MPTP-Induced Parkinson’s Disease." Nutrients 15, no. 4 (February 13, 2023): 930. http://dx.doi.org/10.3390/nu15040930.
Full textAbstract:
Parkinson’s disease (PD) is a prevalent type of neurodegenerative disease. There is mounting evidence that the gut microbiota is involved in the pathogenesis of PD. Sodium butyrate (NaB) can regulate gut microbiota and improve brain functioning in neurological disorders. Hence, we examined whether the neuroprotective function of NaB on PD was mediated by the modulation of gut microbial dysbiosis and revealed its possible mechanisms. Mice were administered 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) for 7 consecutive days to construct the PD model. NaB gavage was given 2 h after the daily MPTP injections for 21 days. NaB improved the motor functioning of PD mice, increased striatal neurotransmitter levels, and reduced the death of dopaminergic neurons. The 16S rRNA sequencing analysis revealed that NaB restored the gut microbial dysbiosis. NaB also attenuated the intestinal barrier’s disruption and reduced serum, colon, and striatal pro-inflammatory cytokines, along with inhibiting the overactivation of glial cells, suggesting an inhibitory effect on inflammation from NaB throughout the gut–brain axis of the PD mice. Mechanistic studies revealed that NaB treatment suppressed the TLR4/MyD88/NF-kB pathway in the colon and striatum. In summary, NaB had a neuroprotective impact on the PD mice, likely linked to its regulation of gut microbiota to inhibit gut–brain axis inflammation.
20
Bowe, W., N. B. Patel, and A. C. Logan. "Acne vulgaris, probiotics and the gut-brain-skin axis: from anecdote to translational medicine." Beneficial Microbes 5, no. 2 (June 1, 2014): 185–99. http://dx.doi.org/10.3920/bm2012.0060.
Full textAbstract:
Acne vulgaris has long been postulated to feature a gastrointestinal mechanism, dating back 80 years to dermatologists John H. Stokes and Donald M. Pillsbury. They hypothesised that emotional states (e.g. depression and anxiety) could alter normal intestinal microbiota, increase intestinal permeability, and contribute to systemic inflammation. They were also among the first to propose the use of probiotic Lactobacillus acidophilus cultures. In recent years, aspects of this gut-brain-skin theory have been further validated via modern scientific investigations. It is evident that gut microbes and oral probiotics could be linked to the skin, and particularly acne severity, by their ability to influence systemic inflammation, oxidative stress, glycaemic control, tissue lipid content, and even mood. This intricate relationship between gut microbiota and the skin may also be influenced by diet, a current area of intense scrutiny by those who study acne. Here we provide a historical background to the gut-brain-skin theory in acne, followed by a summary of contemporary investigations and clinical implications.
21
Derovs, Aleksejs, Sniedze Laivacuma, and Angelika Krumina. "Targeting Microbiota: What Do We Know about It at Present?" Medicina 55, no. 8 (August 10, 2019): 459. http://dx.doi.org/10.3390/medicina55080459.
Full textAbstract:
The human microbiota is a variety of different microorganisms. The composition of microbiota varies from host to host, and it changes during the lifetime. It is known that microbiome may be changed because of a diet, bacteriophages and different processes for example, such as inflammation. Like all other areas of medicine, there is a continuous growth in the area of microbiology. Different microbes can reside in all sites of a human body, even in locations that were previously considered as sterile; for example, liver, pancreas, brain and adipose tissue. Presently one of the etiological factors for liver disease is considered to be pro-inflammatory changes in a host’s organism. There are lot of supporting data about intestinal dysbiosis and increased intestinal permeability and its effect on development of liver disease pointing to the gut–liver axis. The gut–liver axis affects pathogenesis of many liver diseases, such as chronic hepatitis B, chronic hepatitis C, alcoholic liver disease, non-alcoholic liver disease, non-alcoholic steatohepatitis, liver cirrhosis and hepatocellular carcinoma. Gut microbiota has been implicated in the regulation of brain health, emphasizing the gut–brain axis. Also, experiments with mice showed that microorganisms have significant effects on the blood–brain barrier integrity. Microbiota can modulate a variety of mechanisms through the gut–liver axis and gut–brain axis. Normal intestinal flora impacts the health of a host in many positive ways, but there is now significant evidence that intestinal microbiota, especially altered, have the ability to impact the pathologies of many diseases through different inflammatory mechanisms. At this point, many of the pathophysiological reactions in case of microbial disbyosis are still unclear.
22
Seitz, Jochen, Brigitte Dahmen, Lara Keller, and Beate Herpertz-Dahlmann. "Gut Feelings: How Microbiota Might Impact the Development and Course of Anorexia Nervosa." Nutrients 12, no. 11 (October 28, 2020): 3295. http://dx.doi.org/10.3390/nu12113295.
Full textAbstract:
Anorexia nervosa (AN) can probably be regarded as a “model” for studying the interaction of nutrition with the gut–brain axis, which has drawn increased attention from researchers and clinicians alike. The gut microbiota influences somatic effects, such as energy extraction from food and body weight gain, as well as appetite, gut permeability, inflammation and complex psychological behaviors, such as depression or anxiety, all of which play important roles in AN. As nutrition is one of the main factors that influence the gut microbiota, nutritional restriction and selective eating in AN are likely influencing factors; however, nutritional rehabilitation therapy is surprisingly understudied. Here, we review the general mechanisms of the interactions between nutrition, the gut microbiota and the host that may be relevant to AN, paying special attention to the gut–brain axis, and we present the first specific findings in patients with AN and corresponding animal models. In particular, nutritional interventions, including food selection, supplements, and pre-, pro- and synbiotics that have the potential to influence the gut microbiota, are important research targets to potentially support future AN therapy.
23
Manosso, Luana M., Camila O. Arent, Laura A. Borba, Luciane B. Ceretta, João Quevedo, and Gislaine Z. Réus. "Microbiota-Gut-Brain Communication in the SARS-CoV-2 Infection." Cells 10, no. 8 (August 6, 2021): 1993. http://dx.doi.org/10.3390/cells10081993.
Full textAbstract:
The coronavirus disease of 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome 2 (SARS-CoV-2). In addition to pneumonia, individuals affected by the disease have neurological symptoms. Indeed, SARS-CoV-2 has a neuroinvasive capacity. It is known that the infection caused by SARS-CoV-2 leads to a cytokine storm. An exacerbated inflammatory state can lead to the blood–brain barrier (BBB) damage as well as to intestinal dysbiosis. These changes, in turn, are associated with microglial activation and reactivity of astrocytes that can promote the degeneration of neurons and be associated with the development of psychiatric disorders and neurodegenerative diseases. Studies also have been shown that SARS-CoV-2 alters the composition and functional activity of the gut microbiota. The microbiota-gut-brain axis provides a bidirectional homeostatic communication pathway. Thus, this review focuses on studies that show the relationship between inflammation and the gut microbiota–brain axis in SARS-CoV-2 infection.
24
Tang, Yong, Qi Wang, and Jie Liu. "Microbiota-gut-brain axis: A novel potential target of ketogenic diet for epilepsy." Current Opinion in Pharmacology 61 (December 2021): 36–41. http://dx.doi.org/10.1016/j.coph.2021.08.018.
Full text
25
Meng, Lanxia, Xin Yuan, Xuebing Cao, and Zhentao Zhang. "The gut-brain axis in the pathogenesis of Parkinson’s disease." Brain Science Advances 5, no. 2 (June 2019): 73–81. http://dx.doi.org/10.1177/2096595820902566.
Full textAbstract:
Parkinson’s disease (PD) is the second most common neurodegenerative disease. Its pathological markers include Lewy bodies and Lewy neuritis, which primarily affect the substantia nigra. However, in recent years, mounting evidence suggests that PD is a multifocal neurodegenerative process that influences several neuronal structures aside from the substantia nigra, one of which is the enteric nervous system. Many clinical studies have reported that patients with PD experience gastrointestinal dysfunction for many years before the onset of motor symptoms. Emerging evidence indicates that α-synuclein deposition may start in the enteric nervous system and then propagate to the central nervous system. The gut-brain axis plays an important role in PD pathogenesis. Recent evidence suggests that these interactions may be primarily affected by the intestinal microbiota. In this review, the authors discuss recent research, and illustrate how changes in the composition of the gut microbiota may trigger inflammation, thus contributing to neurodegeneration in PD.
26
Sajdel-Sulkowska, Elizabeth M. "Neuropsychiatric Ramifications of COVID-19: Short-Chain Fatty Acid Deficiency and Disturbance of Microbiota-Gut-Brain Axis Signaling." BioMed Research International 2021 (October 5, 2021): 1–15. http://dx.doi.org/10.1155/2021/7880448.
Full textAbstract:
COVID-19-associated neuropsychiatric complications are soaring. There is an urgent need to understand the link between COVID-19 and neuropsychiatric disorders. To that end, this article addresses the premise that SARS-CoV-2 infection results in gut dysbiosis and an altered microbiota-gut-brain (MGB) axis that in turn contributes to the neuropsychiatric ramifications of COVID-19. Altered MGB axis activity has been implicated independently as a risk of neuropsychiatric disorders. A review of the changes in gut microbiota composition in individual psychiatric and neurological disorders and gut microbiota in COVID-19 patients revealed a shared “microbial signature” characterized by a lower microbial diversity and richness and a decrease in health-promoting anti-inflammatory commensal bacteria accompanied by an increase in opportunistic proinflammatory pathogens. Notably, there was a decrease in short-chain fatty acid (SCFA) producing bacteria. SCFAs are key bioactive microbial metabolites with anti-inflammatory functions and have been recognized as a critical signaling pathway in the MGB axis. SCFA deficiency is associated with brain inflammation, considered a cardinal feature of neuropsychiatric disorders. The link between SARS-CoV-2 infection, gut dysbiosis, and altered MGB axis is further supported by COVID-19-associated gastrointestinal symptoms, a high number of SARS-CoV-2 receptors, angiotensin-cleaving enzyme-2 (ACE-2) in the gut, and viral presence in the fecal matter. The binding of SARS-CoV-2 to the receptor results in ACE-2 deficiency that leads to decreased transport of vital dietary components, gut dysbiosis, proinflammatory gut status, increased permeability of the gut-blood barrier (GBB), and systemic inflammation. More clinical research is needed to substantiate further the linkages described above and evaluate the potential significance of gut microbiota as a diagnostic tool. Meanwhile, it is prudent to propose changes in dietary recommendations in favor of a high fiber diet or supplementation with SCFAs or probiotics to prevent or alleviate the neuropsychiatric ramifications of COVID-19.
27
Sajdel-Sulkowska, Elizabeth M. "Neuropsychiatric Ramifications of COVID-19: Short-Chain Fatty Acid Deficiency and Disturbance of Microbiota-Gut-Brain Axis Signaling." BioMed Research International 2021 (October 5, 2021): 1–15. http://dx.doi.org/10.1155/2021/7880448.
Full textAbstract:
COVID-19-associated neuropsychiatric complications are soaring. There is an urgent need to understand the link between COVID-19 and neuropsychiatric disorders. To that end, this article addresses the premise that SARS-CoV-2 infection results in gut dysbiosis and an altered microbiota-gut-brain (MGB) axis that in turn contributes to the neuropsychiatric ramifications of COVID-19. Altered MGB axis activity has been implicated independently as a risk of neuropsychiatric disorders. A review of the changes in gut microbiota composition in individual psychiatric and neurological disorders and gut microbiota in COVID-19 patients revealed a shared “microbial signature” characterized by a lower microbial diversity and richness and a decrease in health-promoting anti-inflammatory commensal bacteria accompanied by an increase in opportunistic proinflammatory pathogens. Notably, there was a decrease in short-chain fatty acid (SCFA) producing bacteria. SCFAs are key bioactive microbial metabolites with anti-inflammatory functions and have been recognized as a critical signaling pathway in the MGB axis. SCFA deficiency is associated with brain inflammation, considered a cardinal feature of neuropsychiatric disorders. The link between SARS-CoV-2 infection, gut dysbiosis, and altered MGB axis is further supported by COVID-19-associated gastrointestinal symptoms, a high number of SARS-CoV-2 receptors, angiotensin-cleaving enzyme-2 (ACE-2) in the gut, and viral presence in the fecal matter. The binding of SARS-CoV-2 to the receptor results in ACE-2 deficiency that leads to decreased transport of vital dietary components, gut dysbiosis, proinflammatory gut status, increased permeability of the gut-blood barrier (GBB), and systemic inflammation. More clinical research is needed to substantiate further the linkages described above and evaluate the potential significance of gut microbiota as a diagnostic tool. Meanwhile, it is prudent to propose changes in dietary recommendations in favor of a high fiber diet or supplementation with SCFAs or probiotics to prevent or alleviate the neuropsychiatric ramifications of COVID-19.
28
Suda, Kazunori, and Kazunori Matsuda. "How Microbes Affect Depression: Underlying Mechanisms via the Gut–Brain Axis and the Modulating Role of Probiotics." International Journal of Molecular Sciences 23, no. 3 (January 21, 2022): 1172. http://dx.doi.org/10.3390/ijms23031172.
Full textAbstract:
Accumulating evidence suggests that the gut microbiome influences the brain functions and psychological state of its host via the gut–brain axis, and gut dysbiosis has been linked to several mental illnesses, including major depressive disorder (MDD). Animal experiments have shown that a depletion of the gut microbiota leads to behavioral changes, and is associated with pathological changes, including abnormal stress response and impaired adult neurogenesis. Short-chain fatty acids such as butyrate are known to contribute to the up-regulation of brain-derived neurotrophic factor (BDNF), and gut dysbiosis causes decreased levels of BDNF, which could affect neuronal development and synaptic plasticity. Increased gut permeability causes an influx of gut microbial components such as lipopolysaccharides, and the resultant systemic inflammation may lead to neuroinflammation in the central nervous system. In light of the fact that gut microbial factors contribute to the initiation and exacerbation of depressive symptoms, this review summarizes the current understanding of the molecular mechanisms involved in MDD onset, and discusses the therapeutic potential of probiotics, including butyrate-producing bacteria, which can mediate the microbiota–gut–brain axis.
29
Niazi, Madiha Khan, Farooq Hassan, Tabussam Tufail, Muhammad Amjed ismail, and Khadija Riaz. "The Role of Microbiome in Psychiatric Diseases (Insomnia and Anxiety/Depression) with Microbiological Mechanisms." Advanced Gut & Microbiome Research 2023 (February 20, 2023): 1–9. http://dx.doi.org/10.1155/2023/1566684.
Full textAbstract:
More focus is being paid to the relationship between gastrointestinal microbiota and human health. The microbiota-gut-brain axis was created as a result of the intricate networks and connections between the gastrointestinal bacteria and the host, highlighting the significant impact that this environment may have on brain health and central nervous system problems. To communicate with the central nervous system, the gastrointestinal, autonomic, immune, neuroendocrine, and neuroendocrine systems engage in a bidirectional interaction with the microbiota. Through a number of neurological processes, including stimulation of the altered neurotransmitter function, hypothalamic-pituitary-adrenal axis, and immune system activity, changes in this network may have an impact on both health and sickness. Anxiety and sadness are two neuropsychiatric conditions that may be impacted by the microbiota-gut-brain axis, according to a recent study. Numerous host disorders, including obesity, diabetes, and inflammation, have already been related to alterations in the gut microbiota’s makeup. In this article, the effects of the gut microbiota on the functioning of the central nervous system are examined, with a focus on the symptoms of anxiety and depression. After examining how stress affects the autonomic, neuroendocrine, immunological, and neurotransmitter systems, modern gastrointestinal-based therapies stress the importance of the microbiome in the prevention and treatment of brain-based diseases including anxiety and depression.
30
Obrenovich, Mark, Hayden Jaworski, Tara Tadimalla, Adil Mistry, Lorraine Sykes, George Perry, and Robert Bonomo. "The Role of the Microbiota–Gut–Brain Axis and Antibiotics in ALS and Neurodegenerative Diseases." Microorganisms 8, no. 5 (May 23, 2020): 784. http://dx.doi.org/10.3390/microorganisms8050784.
Full textAbstract:
The human gut hosts a wide and diverse ecosystem of microorganisms termed the microbiota, which line the walls of the digestive tract and colon where they co-metabolize digestible and indigestible food to contribute a plethora of biochemical compounds with diverse biological functions. The influence gut microbes have on neurological processes is largely yet unexplored. However, recent data regarding the so-called leaky gut, leaky brain syndrome suggests a potential link between the gut microbiota, inflammation and host co-metabolism that may affect neuropathology both locally and distally from sites where microorganisms are found. The focus of this manuscript is to draw connection between the microbiota–gut–brain (MGB) axis, antibiotics and the use of “BUGS AS DRUGS” for neurodegenerative diseases, their treatment, diagnoses and management and to compare the effect of current and past pharmaceuticals and antibiotics for alternative mechanisms of action for brain and neuronal disorders, such as Alzheimer disease (AD), Amyotrophic Lateral Sclerosis (ALS), mood disorders, schizophrenia, autism spectrum disorders and others. It is a paradigm shift to suggest these diseases can be largely affected by unknown aspects of the microbiota. Therefore, a future exists for applying microbial, chemobiotic and chemotherapeutic approaches to enhance translational and personalized medical outcomes. Microbial modifying applications, such as CRISPR technology and recombinant DNA technology, among others, echo a theme in shifting paradigms, which involve the gut microbiota (GM) and mycobiota and will lead to potential gut-driven treatments for refractory neurologic diseases.
31
Kohl, Hannah M., Andrea R. Castillo, and Javier Ochoa-Repáraz. "The Microbiome as a Therapeutic Target for Multiple Sclerosis: Can Genetically Engineered Probiotics Treat the Disease?" Diseases 8, no. 3 (August 30, 2020): 33. http://dx.doi.org/10.3390/diseases8030033.
Full textAbstract:
There is an increasing interest in the intestinal microbiota as a critical regulator of the development and function of the immune, nervous, and endocrine systems. Experimental work in animal models has provided the foundation for clinical studies to investigate associations between microbiota composition and function and human disease, including multiple sclerosis (MS). Initial work done using an animal model of brain inflammation, experimental autoimmune encephalomyelitis (EAE), suggests the existence of a microbiota–gut–brain axis connection in the context of MS, and microbiome sequence analyses reveal increases and decreases of microbial taxa in MS intestines. In this review, we discuss the impact of the intestinal microbiota on the immune system and the role of the microbiome–gut–brain axis in the neuroinflammatory disease MS. We also discuss experimental evidence supporting the hypothesis that modulating the intestinal microbiota through genetically modified probiotics may provide immunomodulatory and protective effects as a novel therapeutic approach to treat this devastating disease.
32
Xiromerisiou, Georgia, Chrysoula Marogianni, Anastasia Androutsopoulou, Panagiotis Ntavaroukas, Dimitrios Mysiris, and Stamatia Papoutsopoulou. "Parkinson’s Disease, It Takes Guts: The Correlation between Intestinal Microbiome and Cytokine Network with Neurodegeneration." Biology 12, no. 1 (January 7, 2023): 93. http://dx.doi.org/10.3390/biology12010093.
Full textAbstract:
Parkinson’s disease is a progressive neurodegenerative disorder with motor, physical and behavioral symptoms that can have a profound impact on the patient’s quality of life. Most cases are idiopathic, and the exact mechanism of the disease’s cause is unknown. The current hypothesis focuses on the gut-brain axis and states that gut microbiota dysbiosis can trigger inflammation and advances the development of Parkinson’s disease. This systematic review presents the current knowledge of gut microbiota analysis and inflammation based on selected studies on Parkinson’s patients and experimental animal models. Changes in gut microbiota correlate with Parkinson’s disease, but only a few studies have considered inflammatory modulators as important triggers of the disease. Nevertheless, it is evident that proinflammatory cytokines and chemokines are induced in the gut, the circulation, and the brain before the development of the disease’s neurological symptoms and exacerbate the disease. Increased levels of tumor necrosis factor, interleukin-1β, interleukin-6, interleukin-17A and interferon-γ can correlate with altered gut microbiota. Instead, treatment of gut dysbiosis is accompanied by reduced levels of inflammatory mediators in specific tissues, such as the colon, brain and serum and/or cerebrospinal fluid. Deciphering the role of the immune responses and the mechanisms of the PD-associated gut microbiota will assist the interpretation of the pathogenesis of Parkinson’s and will elucidate appropriate therapeutic strategies.
33
Shabbir, Umair, Akanksha Tyagi, Fazle Elahi, Simon Okomo Aloo, and Deog-Hwan Oh. "The Potential Role of Polyphenols in Oxidative Stress and Inflammation Induced by Gut Microbiota in Alzheimer’s Disease." Antioxidants 10, no. 9 (August 27, 2021): 1370. http://dx.doi.org/10.3390/antiox10091370.
Full textAbstract:
Gut microbiota (GM) play a role in the metabolic health, gut eubiosis, nutrition, and physiology of humans. They are also involved in the regulation of inflammation, oxidative stress, immune responses, central and peripheral neurotransmission. Aging and unhealthy dietary patterns, along with oxidative and inflammatory responses due to gut dysbiosis, can lead to the pathogenesis of neurodegenerative diseases, especially Alzheimer’s disease (AD). Although the exact mechanism between AD and GM dysbiosis is still unknown, recent studies claim that secretions from the gut can enhance hallmarks of AD by disturbing the intestinal permeability and blood–brain barrier via the microbiota–gut–brain axis. Dietary polyphenols are the secondary metabolites of plants that possess anti-oxidative and anti-inflammatory properties and can ameliorate gut dysbiosis by enhancing the abundance of beneficial bacteria. Thus, modulation of gut by polyphenols can prevent and treat AD and other neurodegenerative diseases. This review summarizes the role of oxidative stress, inflammation, and GM in AD. Further, it provides an overview on the ability of polyphenols to modulate gut dysbiosis, oxidative stress, and inflammation against AD.
34
Adamczyk-Sowa, Monika, Aldona Medrek, Paulina Madej, Wirginia Michlicka, and Pawel Dobrakowski. "Does the Gut Microbiota Influence Immunity and Inflammation in Multiple Sclerosis Pathophysiology?" Journal of Immunology Research 2017 (2017): 1–14. http://dx.doi.org/10.1155/2017/7904821.
Full textAbstract:
Aim.Evaluation of the impact of gut microflora on the pathophysiology of MS.Results. The etiopathogenesis of MS is not fully known. Gut microbiota may be of a great importance in the pathogenesis of MS, since recent findings suggest that substitutions of certain microbial population in the gut can lead to proinflammatory state, which can lead to MS in humans. In contrast, other commensal bacteria and their antigenic products may protect against inflammation within the central nervous system. The type of intestinal flora is affected by antibiotics, stress, or diet. The effects on MS through the intestinal microflora can also be achieved by antibiotic therapy andLactobacillus. EAE, as an animal model of MS, indicates a strong influence of the gut microbiota on the immune system and shows that disturbances in gut physiology may contribute to the development of MS.Conclusions.The relationship between the central nervous system, the immune system, and the gut microbiota relates to the influence of microorganisms in the development of MS. A possible interaction between gut microbiota and the immune system can be perceived through regulation by the endocannabinoid system. It may offer an opportunity to understand the interaction comprised in the gut-immune-brain axis.
35
Hutchinson, Ashley N., Lina Tingö, and Robert Jan Brummer. "The Potential Effects of Probiotics and ω-3 Fatty Acids on Chronic Low-Grade Inflammation." Nutrients 12, no. 8 (August 11, 2020): 2402. http://dx.doi.org/10.3390/nu12082402.
Full textAbstract:
Chronic low-grade inflammation negatively impacts health and is associated with aging and obesity, among other health outcomes. A large number of immune mediators are present in the digestive tract and interact with gut bacteria to impact immune function. The gut microbiota itself is also an important initiator of inflammation, for example by releasing compounds such as lipopolysaccharides (LPS) that may influence cytokine production and immune cell function. Certain nutrients (e.g., probiotics, ω-3 fatty acids [FA]) may increase gut microbiota diversity and reduce inflammation. Lactobacilli and Bifidobacteria, among others, prevent gut hyperpermeability and lower LPS-dependent chronic low-grade inflammation. Furthermore, ω-3 FA generate positive effects on inflammation-related conditions (e.g., hypertriglyceridemia, diabetes) by interacting with immune, metabolic, and inflammatory pathways. Ω-3 FA also increase LPS-suppressing bacteria (i.e., Bifidobacteria) and decrease LPS-producing bacteria (i.e., Enterobacteria). Additionally, ω-3 FA appear to promote short-chain FA production. Therefore, combining probiotics with ω-3 FA presents a promising strategy to promote beneficial immune regulation via the gut microbiota, with potential beneficial effects on conditions of inflammatory origin, as commonly experienced by aged and obese individuals, as well as improvements in gut-brain-axis communication.
36
Anand, Nikhilesh, Vasavi Rakesh Gorantla, and Saravana Babu Chidambaram. "The Role of Gut Dysbiosis in the Pathophysiology of Neuropsychiatric Disorders." Cells 12, no. 1 (December 23, 2022): 54. http://dx.doi.org/10.3390/cells12010054.
Full textAbstract:
Mounting evidence shows that the complex gut microbial ecosystem in the human gastrointestinal (GI) tract regulates the physiology of the central nervous system (CNS) via microbiota and the gut–brain (MGB) axis. The GI microbial ecosystem communicates with the brain through the neuroendocrine, immune, and autonomic nervous systems. Recent studies have bolstered the involvement of dysfunctional MGB axis signaling in the pathophysiology of several neurodegenerative, neurodevelopmental, and neuropsychiatric disorders (NPDs). Several investigations on the dynamic microbial system and genetic–environmental interactions with the gut microbiota (GM) have shown that changes in the composition, diversity and/or functions of gut microbes (termed “gut dysbiosis” (GD)) affect neuropsychiatric health by inducing alterations in the signaling pathways of the MGB axis. Interestingly, both preclinical and clinical evidence shows a positive correlation between GD and the pathogenesis and progression of NPDs. Long-term GD leads to overstimulation of hypothalamic–pituitary–adrenal (HPA) axis and the neuroimmune system, along with altered neurotransmitter levels, resulting in dysfunctional signal transduction, inflammation, increased oxidative stress (OS), mitochondrial dysfunction, and neuronal death. Further studies on the MGB axis have highlighted the significance of GM in the development of brain regions specific to stress-related behaviors, including depression and anxiety, and the immune system in the early life. GD-mediated deregulation of the MGB axis imbalances host homeostasis significantly by disrupting the integrity of the intestinal and blood–brain barrier (BBB), mucus secretion, and gut immune and brain immune functions. This review collates evidence on the potential interaction between GD and NPDs from preclinical and clinical data. Additionally, we summarize the use of non-therapeutic modulators such as pro-, pre-, syn- and post-biotics, and specific diets or fecal microbiota transplantation (FMT), which are promising targets for the management of NPDs.
37
Rodriguez-Gonzalez, Alicia, and Laura Orio. "Microbiota and Alcohol Use Disorder: Are Psychobiotics a Novel Therapeutic Strategy?" Current Pharmaceutical Design 26, no. 20 (June 21, 2020): 2426–37. http://dx.doi.org/10.2174/1381612826666200122153541.
Full textAbstract:
In recent years, there has been an exciting focus of research attempting to understand neuropsychiatric disorders from a holistic perspective in order to determine the role of gut microbiota in the aetiology and pathogenesis of such disorders. Thus, the possible therapeutic benefits of targeting gut microbiota are being explored for conditions such as stress, depression or schizophrenia. Growing evidence indicates that there is bidirectional communication between gut microbiota and the brain that has an effect on normal CNS functioning and behavioural responses. Alcohol abuse damages the gastrointestinal tract, alters gut microbiota and induces neuroinflammation and cognitive decline. The relationship between alcohol abuse and hypothalamic-pituitary-adrenal axis activation, inflammation and immune regulation has been well documented. In this review, we explore the connection between microbiota, brain function and behaviour, as well as the mechanisms through which alcohol induces microbiota dysbiosis and intestinal barrier dysfunction. Finally, we propose the study of psychobiotics as a novel pharmaceutical strategy to treat alcohol use disorders.
38
Dehhaghi, Mona, Hamed Kazemi Shariat Panahi, and Gilles J. Guillemin. "Microorganisms, Tryptophan Metabolism, and Kynurenine Pathway: A Complex Interconnected Loop Influencing Human Health Status." International Journal of Tryptophan Research 12 (January 2019): 117864691985299. http://dx.doi.org/10.1177/1178646919852996.
Full textAbstract:
The kynurenine pathway is important in cellular energy generation and limiting cellular ageing as it degrades about 90% of dietary tryptophan into the essential co-factor NAD+ (nicotinamide adenine dinucleotide). Prior to the production of NAD+, various intermediate compounds with neuroactivity (kynurenic acid, quinolinic acid) or antioxidant activity (3-hydroxykynurenine, picolinic acid) are synthesized. The kynurenine metabolites can participate in numerous neurodegenerative disorders (Alzheimer disease, amyotrophic lateral sclerosis, Huntington disease, and Parkinson disease) or other diseases such as AIDS, cancer, cardiovascular diseases, inflammation, and irritable bowel syndrome. Recently, the role of gut in affecting the emotional and cognitive centres of the brain has attracted a great deal of attention. In this review, we focus on the bidirectional communication between the gut and the brain, known as the gut-brain axis. The interaction of components of this axis, namely, the gut, its microbiota, and gut pathogens; tryptophan; the kynurenine pathway on tryptophan availability; the regulation of kynurenine metabolite concentration; and diversity and population of gut microbiota, has been considered.
39
Ringseis, Robert, Denise K. Gessner, and Klaus Eder. "The Gut–Liver Axis in the Control of Energy Metabolism and Food Intake in Animals." Annual Review of Animal Biosciences 8, no. 1 (February 15, 2020): 295–319. http://dx.doi.org/10.1146/annurev-animal-021419-083852.
Full textAbstract:
Recent research has convincingly demonstrated a bidirectional communication axis between the gut and liver that enables the gut microbiota to strongly affect animals’ feeding behavior and energy metabolism. As such, the gut–liver axis enables the host to control and shape the gut microbiota and to protect the intestinal barrier. Gut microbiota–host communication is based on several gut-derived compounds, such as short-chain fatty acids, bile acids, methylamines, amino acid–derived metabolites, and microbial-associated molecular patterns, which act as communication signals, and multiple host receptors, which sense the signals, thereby stimulating signaling and metabolic pathways in all key tissues of energy metabolism and food intake regulation. Disturbance in the microbial ecosystem balance, or microbial dysbiosis, causes profound derangements in the regulation of appetite and satiety in the hypothalamic centers of the brain and in key metabolic pathways in peripheral tissues owing to intestinal barrier disruption and subsequent induction of hepatic and hypothalamic inflammation.
40
Kang, Yongbo, Xing Kang, Hongfang Zhang, Qingqing Liu, Hao Yang, and Weiping Fan. "Gut Microbiota and Parkinson’s Disease: Implications for Faecal Microbiota Transplantation Therapy." ASN Neuro 13 (January 2021): 175909142110162. http://dx.doi.org/10.1177/17590914211016217.
Full textAbstract:
Parkinson's disease (PD) ranks the second place among neurodegenerative diseases in terms of its morbidity, which affects 1-2% people aged over 65 years. In addition to genetics, some environmental factors may exert vital parts in PD occurrence as well. At present, more and more studies are conducted to elucidate the association between gut microbial dysbiosis and the incidence of PD. Gut microbial dysbiosis has a certain effect on both the central nervous system (CNS) and the enteric nervous system (ENS), which indicates that there is a gut-microbiota-brain axis that induces CNS disorders. Some gut microbial strains are suggested to suppress or weaken the neuroinflammation- and gut-inflammation-immune responses, which suggests the protective and pathogenic effects of certain gut microbial species on PD progression. Therefore, gut microbiome may contain plenty of targets for preventing and managing PD. Faecal microbiota transplantation (FMT) may serve as a direct and useful treatment for PD in the future. Nonetheless, there is little available scientific research in this field. The present work reviewed the latest research to examine the association of gut microbiota with PD, and the future prospects of FMT treatment.
41
Pinchaud, Katleen, Zeeshan Hafeez, Sandrine Auger, Jean-Marc Chatel, Sead Chadi, Philippe Langella, Justine Paoli, Annie Dary-Mourot, Katy Maguin-Gaté, and Jean Luc Olivier. "Impact of Dietary Arachidonic Acid on Gut Microbiota Composition and Gut–Brain Axis in Male BALB/C Mice." Nutrients 14, no. 24 (December 15, 2022): 5338. http://dx.doi.org/10.3390/nu14245338.
Full textAbstract:
Although arachidonic acid (ARA) is the precursor of the majority of eicosanoids, its influence as a food component on health is not well known. Therefore, we investigated its impact on the gut microbiota and gut–brain axis. Groups of male BALB/c mice were fed either a standard diet containing 5% lipids (Std-ARA) or 15%-lipid diets without ARA (HL-ARA) or with 1% ARA (HL + ARA) for 9 weeks. Fatty acid profiles of all three diets were the same. The HL-ARA diet favored the growth of Bifidobacterium pseudolongum contrary to the HL + ARA diet that favored the pro-inflammatory Escherichia–Shigella genus in fecal microbiota. Dietary ARA intake induced 4- and 15-fold colic overexpression of the pro-inflammatory markers IL-1β and CD40, respectively, without affecting those of TNFα and adiponectin. In the brain, dietary ARA intake led to moderate overexpression of GFAP in the hippocampus and cortex. Both the hyperlipidic diets reduced IL-6 and IL-12 in the brain. For the first time, it was shown that dietary ARA altered the gut microbiota, led to low-grade colic inflammation, and induced astrogliosis in the brain. Further work is necessary to determine the involved mechanisms.
42
Bulgakova, S., N. Romanchuk, and O. Pomazanova. "Psychoneuroimmunoendocrinology and Immune Homeostasis: Gut-brain Axis, Obesity and Cognitive Function." Bulletin of Science and Practice 6, no. 12 (December 15, 2020): 124–54. http://dx.doi.org/10.33619/2414-2948/61/15.
Full textAbstract:
The new competencies of psychoneuroimmunoendocrinology and psychoneuroimmunology play a strategic role in interdisciplinary science and interdisciplinary planning and decision-making. The introduction of multi-vector neurotechnologies of artificial intelligence and the principles of digital health care will contribute to the development of modern neuroscience and neuromarketing. The availability of innovative technologies, such as next-generation sequencing and correlated bioinformatics tools, allows deeper investigation of the cross-network relationships between the microbiota and human immune responses. Immune homeostasis is the balance between immunological tolerance and inflammatory immune responses — a key feature in the outcome of health or disease. A healthy microbiota is the qualitative and quantitative ratio of diverse microbes of individual organs and systems, maintaining the biochemical, metabolic and immune equilibrium of the macroorganism necessary to preserve human health. Functional foods, healthy biomicrobiota, healthy lifestyle and controlled protective environmental effects, artificial intelligence and electromagnetic information load/overload are responsible for the work of the human immune system and its ability to respond to pandemic attacks in a timely manner. Obesity continues to be one of the main problems of modern health care due to its high prevalence and polymorbidity. In addition to cardiometabolic diseases, lesions of the musculoskeletal system, obese individuals show impaired cognitive functions, have a high risk of developing depression and anxiety. The gut microbiota mediates between environmental influences (food, lifestyle) and the physiology of the host, and its change may partially explain the cross-link between the above pathologies. It is known that Western eating patterns are the main cause of the obesity epidemic, which also contributes to dysbiotic drift of the gut microbiota, which in turn contributes to the development of complications associated with obesity. Experimental studies in animal models and, to a lesser extent in humans, show that microbiota is associated with obesity and may contribute to the endocrine, neurochemical and development of systemic inflammation underlying obesity itself and related diseases. Nevertheless, a number of questions remain at present. Modeling the microbiota-gut-brain axis, provides the brain with information from the gut not only through the nervous system but also through a continuous stream of microbial, endocrine, metabolic and immune messages. The communication network provides important keys to understanding how obesity and diabetes can affect the brain by provoking neuropsychiatric diseases. The literature review is devoted to the analysis of data on the relationship of the gut-brain axis, obesity and cognitive functions, immune homeostasis and new competencies: psychoneuroimmunology and psychoneuroimmunoendocrinology.
43
Xu, Fenghua, Yi Cheng, Guangcong Ruan, Liqin Fan, Yuting Tian, Zhifeng Xiao, Dongfeng Chen, and Yanling Wei. "New pathway ameliorating ulcerative colitis: focus on Roseburia intestinalis and the gut–brain axis." Therapeutic Advances in Gastroenterology 14 (January 2021): 175628482110044. http://dx.doi.org/10.1177/17562848211004469.
Full textAbstract:
Background: The community of gut microbes is a key factor controlling the intestinal barrier that communicates with the nervous system through the gut–brain axis. Based on our clinical data showing that populations of Roseburia intestinalis are dramatically decreased in the gut of patients with ulcerative colitis, we studied the efficacy of a strain belonging to this species in the context of colitis and stress using animal models. Methods: Dextran sulfate sodium was used to induce colitis in rats, which then underwent an enema with R. intestinalis as a treatment. The disease activity index, fecal changes and body weight of rats were recorded to evaluate colitis, while histological and immunohistochemical analyses were carried out to examine colon function, and 16S rRNA sequencing was performed to evaluate the gut microbiota change. Behavioral assays and immunohistochemical staining of brain were performed to assess the effect of R. intestinalis on the gut–brain axis. Results: Colitis-related symptoms in rats were significantly relieved after R. intestinalis enema, and the stool traits and colon length of rats were significantly recovered after treatment. The gut epithelial integrity and intestinal barrier were restored in treated rats, as evidenced by the higher expression of Zo-1 in colon tissues, accompanied by the restoration of gut microbiota. Meanwhile, depressive-like behaviors of rats were reduced after treatment, and laboratory experiments on neuronal cells also showed that IL-6, IL-7 and 5-HT were downregulated by R. intestinalis treatment in both serum and brain tissue, while Iba-1 expression was reduced in treated rats. Conclusions: The administration of R. intestinalis contributes to restoration of the gut microbiota, promoting colon repair and the recovery of gastrointestinal function. These alterations are accompanied by the relief of depressive-like behaviors through a process modulated by the neuronal network and the regulation of inflammation by the gut–brain axis.
44
Guo, Libing, Jiaxin Xu, Yunhua Du, Weibo Wu, Wenjing Nie, Dongliang Zhang, Yuling Luo, et al. "Effects of gut microbiota and probiotics on Alzheimer’s disease." Translational Neuroscience 12, no. 1 (January 1, 2021): 573–80. http://dx.doi.org/10.1515/tnsci-2020-0203.
Full textAbstract:
Abstract Alzheimer’s disease (AD) is a progressive neurodegenerative disease with high morbidity, disability, and fatality rate, significantly increasing the global burden of public health. The failure in drug discovery over the past decades has stressed the urgency and importance of seeking new perspectives. Recently, gut microbiome (GM), with the ability to communicate with the brain bidirectionally through the microbiome–gut–brain axis, has attracted much attention in AD-related studies, owing to their strong associations with amyloids, systematic and focal inflammation, impairment of vascular homeostasis and gut barrier, mitochondrial dysfunction, etc., making the regulation of GM, specifically supplementation of probiotics a promising candidate for AD treatment. This article aims to review the leading-edge knowledge concerning potential roles of GM in AD pathogenesis and of probiotics in its treatment and prevention.
45
Robles-Vera, Iñaki, Néstor de la Visitación, Manuel Sánchez, Manuel Gómez-Guzmán, Rosario Jiménez, Javier Moleón, Cristina González-Correa, et al. "Mycophenolate Improves Brain–Gut Axis Inducing Remodeling of Gut Microbiota in DOCA-Salt Hypertensive Rats." Antioxidants 9, no. 12 (November 28, 2020): 1199. http://dx.doi.org/10.3390/antiox9121199.
Full textAbstract:
Microbiota is involved in the host blood pressure (BP) regulation. The immunosuppressive drug mofetil mycophenolate (MMF) ameliorates hypertension. The present study analyzed whether MMF improves dysbiosis in mineralocorticoid-induced hypertension. Male Wistar rats were assigned to three groups: untreated (CTR), deoxycorticosterone acetate (DOCA)-salt, and DOCA treated with MMF for 4 weeks. MMF treatment reduced systolic BP, improved endothelial dysfunction, and reduced oxidative stress and inflammation in aorta. A clear separation in the gut bacterial community between CTR and DOCA groups was found, whereas the cluster belonging to DOCA-MMF group was found to be intermixed. No changes were found at the phylum level among all experimental groups. MMF restored the elevation in lactate-producing bacteria found in DOCA-salt joined to an increase in the acetate-producing bacteria. MMF restored the percentage of anaerobic bacteria in the DOCA-salt group to values similar to control rats. The improvement of gut dysbiosis was associated with an enhanced colonic integrity and a decreased sympathetic drive in the gut. MMF inhibited neuroinflammation in the paraventricular nuclei in the hypothalamus. This study demonstrates for the first time that MMF reduces gut dysbiosis in DOCA-salt hypertension models. This effect seems to be related to its capacity to improve gut integrity due to reduced sympathetic drive in the gut associated with reduced brain neuroinflammation.
46
Chudzik, Agata, Anna Orzyłowska, Radosław Rola, and Greg J. Stanisz. "Probiotics, Prebiotics and Postbiotics on Mitigation of Depression Symptoms: Modulation of the Brain–Gut–Microbiome Axis." Biomolecules 11, no. 7 (July 7, 2021): 1000. http://dx.doi.org/10.3390/biom11071000.
Full textAbstract:
The brain–gut–microbiome axis is a bidirectional communication pathway between the gut microbiota and the central nervous system. The growing interest in the gut microbiota and mechanisms of its interaction with the brain has contributed to the considerable attention given to the potential use of probiotics, prebiotics and postbiotics in the prevention and treatment of depressive disorders. This review discusses the up-to-date findings in preclinical and clinical trials regarding the use of pro-, pre- and postbiotics in depressive disorders. Studies in rodent models of depression show that some of them inhibit inflammation, decrease corticosterone level and change the level of neurometabolites, which consequently lead to mitigation of the symptoms of depression. Moreover, certain clinical studies have indicated improvement in mood as well as changes in biochemical parameters in patients suffering from depressive disorders.
47
Natale, Gianfranco, Francesca Biagioni, Carla Letizia Busceti, Stefano Gambardella, Fiona Limanaqi, and Francesco Fornai. "TREM Receptors Connecting Bowel Inflammation to Neurodegenerative Disorders." Cells 8, no. 10 (September 21, 2019): 1124. http://dx.doi.org/10.3390/cells8101124.
Full textAbstract:
Alterations in Triggering Receptors Expressed on Myeloid cells (TREM-1/2) are bound to a variety of infectious, sterile inflammatory, and degenerative conditions, ranging from inflammatory bowel disease (IBD) to neurodegenerative disorders. TREMs are emerging as key players in pivotal mechanisms often concurring in IBD and neurodegeneration, namely microbiota dysbiosis, leaky gut, and inflammation. In conditions of dysbiosis, compounds released by intestinal bacteria activate TREMs on macrophages, leading to an exuberant pro-inflammatory reaction up to damage in the gut barrier. In turn, TREM-positive activated macrophages along with inflammatory mediators may reach the brain through the blood, glymphatic system, circumventricular organs, or the vagus nerve via the microbiota-gut-brain axis. This leads to a systemic inflammatory response which, in turn, impairs the blood-brain barrier, while promoting further TREM-dependent neuroinflammation and, ultimately, neural injury. Nonetheless, controversial results still exist on the role of TREM-2 compared with TREM-1, depending on disease specificity, stage, and degree of inflammation. Therefore, the present review aimed to provide an update on the role of TREMs in the pathophysiology of IBD and neurodegeneration. The evidence here discussed the highlights of the potential role of TREMs, especially TREM-1, in bridging inflammatory processes in intestinal and neurodegenerative disorders.
48
Del Toro-Barbosa, Mariano, Alejandra Hurtado-Romero, Luis Eduardo Garcia-Amezquita, and Tomás García-Cayuela. "Psychobiotics: Mechanisms of Action, Evaluation Methods and Effectiveness in Applications with Food Products." Nutrients 12, no. 12 (December 19, 2020): 3896. http://dx.doi.org/10.3390/nu12123896.
Full textAbstract:
The gut-brain-microbiota axis consists of a bilateral communication system that enables gut microbes to interact with the brain, and the latter with the gut. Gut bacteria influence behavior, and both depression and anxiety symptoms are directly associated with alterations in the microbiota. Psychobiotics are defined as probiotics that confer mental health benefits to the host when ingested in a particular quantity through interaction with commensal gut bacteria. The action mechanisms by which bacteria exert their psychobiotic potential has not been completely elucidated. However, it has been found that these bacteria provide their benefits mostly through the hypothalamic-pituitary-adrenal (HPA) axis, the immune response and inflammation, and through the production of neurohormones and neurotransmitters. This review aims to explore the different approaches to evaluate the psychobiotic potential of several bacterial strains and fermented products. The reviewed literature suggests that the consumption of psychobiotics could be considered as a viable option to both look after and restore mental health, without undesired secondary effects, and presenting a lower risk of allergies and less dependence compared to psychotropic drugs.
49
Xu, Kaiyu, Xuxuan Gao, Genghong Xia, Muxuan Chen, Nianyi Zeng, Shan Wang, Chao You, et al. "Rapid gut dysbiosis induced by stroke exacerbates brain infarction in turn." Gut 70, no. 8 (February 8, 2021): 1486–94. http://dx.doi.org/10.1136/gutjnl-2020-323263.
Full textAbstract:
ObjectiveStroke is a leading cause of death and disability worldwide. Neuroprotective approaches have failed in clinical trials, thus warranting therapeutic innovations with alternative targets. The gut microbiota is an important contributor to many risk factors for stroke. However, the bidirectional interactions between stroke and gut microbiota remain largely unknown.DesignWe performed two clinical cohort studies to capture the gut dysbiosis dynamics after stroke and their relationship with stroke prognosis. Then, we used a middle cerebral artery occlusion model to explore gut dysbiosis post-stroke in mice and address the causative relationship between acute ischaemic stroke and gut dysbiosis. Finally, we tested whether aminoguanidine, superoxide dismutase and tungstate can alleviate post-stroke brain infarction by restoring gut dysbiosis.ResultsBrain ischaemia rapidly induced intestinal ischaemia and produced excessive nitrate through free radical reactions, resulting in gut dysbiosis with Enterobacteriaceae expansion. Enterobacteriaceae enrichment exacerbated brain infarction by enhancing systemic inflammation and is an independent risk factor for the primary poor outcome of patients with stroke. Administering aminoguanidine or superoxide dismutase to diminish nitrate generation or administering tungstate to inhibit nitrate respiration all resulted in suppressed Enterobacteriaceae overgrowth, reduced systemic inflammation and alleviated brain infarction. These effects were gut microbiome dependent and indicated the translational value of the brain–gut axis in stroke treatment.ConclusionsThis study reveals a reciprocal relationship between stroke and gut dysbiosis. Ischaemic stroke rapidly triggers gut microbiome dysbiosis with Enterobacteriaceae overgrowth that in turn exacerbates brain infarction.
50
Luca, Maria, Maurizio Di Mauro, Marco Di Mauro, and Antonina Luca. "Gut Microbiota in Alzheimer’s Disease, Depression, and Type 2 Diabetes Mellitus: The Role of Oxidative Stress." Oxidative Medicine and Cellular Longevity 2019 (April 17, 2019): 1–10. http://dx.doi.org/10.1155/2019/4730539.
Full textAbstract:
Gut microbiota consists of over 100 trillion microorganisms including at least 1000 different species of bacteria and is crucially involved in physiological and pathophysiological processes occurring in the host. An imbalanced gastrointestinal ecosystem (dysbiosis) seems to be a contributor to the development and maintenance of several diseases, such as Alzheimer’s disease, depression, and type 2 diabetes mellitus. Interestingly, the three disorders are frequently associated as demonstrated by the high comorbidity rates. In this review, we introduce gut microbiota and its role in both normal and pathological processes; then, we discuss the importance of the gut-brain axis as well as the role of oxidative stress and inflammation as mediators of the pathological processes in which dysbiosis is involved. Specific sections pertain the role of the altered gut microbiota in the pathogenesis of Alzheimer’s disease, depression, and type 2 diabetes mellitus. The therapeutic implications of microbiota manipulation are briefly discussed. Finally, a conclusion comments on the possible role of dysbiosis as a common pathogenetic contributor (via oxidative stress and inflammation) shared by the three disorders.