Journal of Cellular Neuroscience and Oxidative Stress最新文献_第8页

Calcium imaging techniques in cell lines 细胞系钙成像技术

Journal of Cellular Neuroscience and Oxidative Stress Pub Date : 2018-08-18 DOI: 10.37212/jcnos.609922

L. Pecze

{"title":"Calcium imaging techniques in cell lines","authors":"L. Pecze","doi":"10.37212/jcnos.609922","DOIUrl":"https://doi.org/10.37212/jcnos.609922","url":null,"abstract":"Calcium imaging is a scientific technique which is designed to measure the intracellular free calcium concentration (Ca2+) in an isolated cell or tissue. Calcium imaging techniques utilizes fluorescent molecules so called Ca2+ indicators that can respond to the binding of Ca2+ ions by changing heir fluorescence properties. Binding of a Ca2+ ion to a fluorescent indicator molecule leads to either an elevation in its fluorescence intensity or emission/excitation wavelength shift. Two main classes of calcium indicators are chemical indicators and genetically encoded calcium indicators. Chemical indicators are small molecules that can bind calcium ions. This group of indicators includes Fura-2, Fluo-3, Fluo-4, Rhod-2. These dyes are often used with acetoxymethyl esters, in order to render the molecule lipophilic and to allow easy entrance into the cell. Genetically encoded indicators do not need to be loaded onto cells, instead the genes encoding for these proteins can be easily transfected to cells. These indicators are fluorescent proteins derived from green fluorescent protein (GFP). The time-scan mode of laser confocal microscopy is often used for calcium imaging. Intracellular Ca 2+ ions generate versatile intracellular signals that control key functions in all types of cells. In sensory neurons Ca2+ signals are associated with pain transmission.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46226517","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Intravenous NAD+ effectively increased the NAD metabolome, reduced oxidative stress and inflammation, and increased expression of longevity genes safely in elderly humans 静脉注射NAD+有效增加老年人NAD代谢组，减少氧化应激和炎症，并安全地增加长寿基因的表达

Journal of Cellular Neuroscience and Oxidative Stress Pub Date : 2018-08-18 DOI: 10.37212/JCNOS.610084

N. Braidy

{"title":"Intravenous NAD+ effectively increased the NAD metabolome, reduced oxidative stress and inflammation, and increased expression of longevity genes safely in elderly humans","authors":"N. Braidy","doi":"10.37212/JCNOS.610084","DOIUrl":"https://doi.org/10.37212/JCNOS.610084","url":null,"abstract":"Nicotinamide adenine dinucleotide (NAD+) serves important roles in hydrogen transfer and as the cosubstrate for poly(ADP-ribose) polymerase (PARPs), the sirtuin (SIRT1-7) family of enzymes, and CD38 glycohydrolases. Recently, intravenous (IV) NAD+ therapy has been used as a holistic approach to treat withdrawal from addiction, overcome anxiety and depression, and improve overall quality of life with minimal symptoms between 3-7 days of treatment. We evaluated repeat dose IV NAD+ (1000 mg) for 6 days in a population of 8 healthy adults between the ages of 70 and 80 years. Our data is the first to show that IV NAD+ increases the blood NAD+ metabolome in elderly humans. We found increased concentrations of glutathione peroxidase -3 and paraoxonase-1, and decreased concentrations of 8-iso-prostaglandin F2α, advanced oxidative protein products, protein carbonyl, C-reactive protein and interleukin 6. We report significant increases in mRNA expression and activity of SIRT1, and Forkhead box O1, and reduced acetylated p53 in peripheral blood mononuclear cells isolated from these subjects. No major adverse effects were reported in this study. The study shows that repeat IV dose of NAD+ is a safe and efficient way to slow down age-related decline in NAD+.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45745097","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Neurodegenerative disease and microbiota 神经退行性疾病与微生物群

Journal of Cellular Neuroscience and Oxidative Stress Pub Date : 2018-08-18 DOI: 10.37212/jcnos.610095

O. Akpınar

{"title":"Neurodegenerative disease and microbiota","authors":"O. Akpınar","doi":"10.37212/jcnos.610095","DOIUrl":"https://doi.org/10.37212/jcnos.610095","url":null,"abstract":"Evidence suggests that intestinal microbiota, especially in the case of dysbiosis, may affect the progression of neurological diseases and may even lead to the formation of the disease. It has been realized that decreasing diversity in aging gut of the microbiota may be an important factor in the development of neurodegeneration. Neuroinflammation is one of the major mechanisms that associate microbiota with agerelated diseases. Intestinal microbiota; plays a key role in the activation of microglia and it is suggested that manipulation of intestinal microbiota, especially with short chain fatty acid producing bacteria, may modulate neuroimmun activation (Westfall et al. 2017). On the clinical and scientific level, most neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. Disease related pathology may spread across the nervous system in a self-propagative fashion. Importantly, there is a strong bidirectional interaction between gut microbiota and the central nervous system, a connection recently termed the “microbiota-gut-brainaxis” (Jiang et al. 2017; Houser and Tansey, 2017). While the effects of the autonomic nervous system on gut physiology have been known for a long time, we are just beginning to understand that gut microbiota has strong effects on CNS physiology as well. The vast number of ways through which gut microbiota affects the host shows intriguing overlaps with pathways previously implicated in neurodegeneration. Although evidence for involvement of microbiota in neurodegenerative diseases is still very preliminary, initial findings are extremely promising (Zhu et al. 2017). This presentation will give an overview of recent findings regarding the connections between gutmicrobiota and neurodegenerative disorders and how this may reshape our understanding of these diseases.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46562767","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Traumatic brain injury models in rats 大鼠创伤性脑损伤模型

Journal of Cellular Neuroscience and Oxidative Stress Pub Date : 2018-08-18 DOI: 10.37212/jcnos.610092

Kemal Ertilav

{"title":"Traumatic brain injury models in rats","authors":"Kemal Ertilav","doi":"10.37212/jcnos.610092","DOIUrl":"https://doi.org/10.37212/jcnos.610092","url":null,"abstract":"Traumatic brain injury (TBI) is induced in the brain by external forces such as traffic accidents and heat trauma. Death and disability are induced by the TBI. Indeed, worldwide, about 10 million people are annually deaths or hospitalizations annually by the TBI exposures. In addition, about 57 million exposed to brain injury after TBI annually (Xiong et al. 2013). There is no direct treatment method for the TBI. After the TBI, different pathological processes such as oxidative stress, inflammation and apoptosis are induced by the brain injury. Hence, investigations of new treatment methods in rodent models have important role for inhibition of the pathological processes of human. Marmarou method has been used to make a diffuse head trauma (Marmarou et al. 1994) and it is popular for induction of TBI in rats. Before induction of TBI, the animals should anesthetized by anesthetics such as ketamine and xylazine combination. The animals are placed in prone position on the trauma table under the anesthesia. After skin incision, a steel disc (10 mm X 3 mm) is placed midline between coronal and lambdoid sutures on the animal’s skull, and a 250-300 g weight is freely dropped through a cylindrical tube, with 19 mm inner diameter, from 2 m height onto the head of the animal (Marmarou et al. 1994). In the presentation, a selection of the principal models is described and the model was compared","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46794731","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The gut-brain axis: interactions between microbiota and nervous systems 肠脑轴：微生物群和神经系统之间的相互作用

Journal of Cellular Neuroscience and Oxidative Stress Pub Date : 2018-08-18 DOI: 10.37212/JCNOS.610103

O. Akpınar

{"title":"The gut-brain axis: interactions between microbiota and nervous systems","authors":"O. Akpınar","doi":"10.37212/JCNOS.610103","DOIUrl":"https://doi.org/10.37212/JCNOS.610103","url":null,"abstract":"Humans coexist in a mutualistic relationship with the intestinal microbiota, a complex microbial ecosystem that resides largely in the distal bowel. The lower gastrointestinal tract contains almost 100 trillion microorganisms, most of which are bacteria. More than 1,000 bacterial species have been identified in this microbiota. The intestinal microbiota lives in a symbiotic relationship with the host. A bidirectional neurohumoral communication system, known as the gut–brain axis, integrates the host gut and brain activities (Mayer et al. 2015). Communication between the brain and gut occurs along a network of pathways collectively termed the brain-gut axis. The brain-gut axis encompass the CNS, ENS, sympathetic and parasympathetic branches of the autonomic nervous system, neuroendocrine and neuroimmune pathways, and the gut microbiota (Colins et al. 2012). The gut microbiota can signal to the brain via a number of pathways which include: regulating immune activity and the production of roinflammatory cytokines that can either stimulate the HPA axis to produce CRH, ACTH and cortisol, or directly impact on CNS immune activity; through the production of SCFAs such as propionate, butyrate, and acetate; the production of neurotransmitters which may enter circulation and cross the blood brain barrier; by modulating tryptophan metabolism and downstream metabolites, serotonin, kynurenic acid and quinolinic acid. Neuronal and spinal pathways, particularly afferent signaling pathways of the vagus nerve, are critical in mediating the effect of the gut microbiota on brain function and behavior. Microbial produced SCFAs and indole also impact on EC cells of the enteric nervous system (Romijn et al. 2008; Cani et al. 2013). The purpose of this presentation was to summarize our current knowledge regarding the role of microbiota in bottom-up pathways of communication in the gutbrain axis.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44445093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

Cerebral ischemia models in rats 大鼠脑缺血模型

Journal of Cellular Neuroscience and Oxidative Stress Pub Date : 2018-08-18 DOI: 10.37212/jcnos.610115

Zeki Serdar Ataizi

{"title":"Cerebral ischemia models in rats","authors":"Zeki Serdar Ataizi","doi":"10.37212/jcnos.610115","DOIUrl":"https://doi.org/10.37212/jcnos.610115","url":null,"abstract":"Stroke is the second cause of death worldwide. Stroke induces cerebral ischemia. The cerebral ischemia is a neurodegenerative disease that causes disability and mortality. An accumulating body of evidence indicates that abnormalities of Ca2+ homeostasis are caused by excessive levels of free oxygen radicals in rats with cerebral ischemia. Occlusion of middle cerebral artery in human induces cerebral ischemic stroke. In experimental animals, best model of induction of cerebral ischemic stroke is occlusion of middle cerebral artery for 30 min (Canazza et al. 2014). In cerebral ischemia stoke model, right or left middle cerebral artery is exposed through a ventral midline incision in the neck and it is loosely encircled with sutures for further occlusion. Following a midline incision, the skull is craniectomized to expose the right or left common carotid artery. A 3-0 suture is positioned so that it encircled the middle cerebral artery for further occlusion. Cerebral ischemic surgery is performed through occlusion of the right or left middle cerebral artery for 30 min (Akpinar et al. 2016). In addition to the best model, there are also other models of cerebral stroke in rodents such as the intra-luminal suture, thromboembolic, the coagulation or ligation, the endothelin-1, and the distal artery compression models (Canazza et al. 2014). In the presentation, a selection of the principal models is described and the model was compared with the other models.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43232881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Effects of cell phone (900 and 1800 MHz) and Wi-Fi (2450 MHz) frequencies on oxidative stress in laryngeal mucosa 手机（900和1800 MHz）和Wi-Fi（2450 MHz）频率对喉粘膜氧化应激的影响

Journal of Cellular Neuroscience and Oxidative Stress Pub Date : 2018-08-18 DOI: 10.37212/JCNOS.610132

S. G. Kütük

{"title":"Effects of cell phone (900 and 1800 MHz) and Wi-Fi (2450 MHz) frequencies on oxidative stress in laryngeal mucosa","authors":"S. G. Kütük","doi":"10.37212/JCNOS.610132","DOIUrl":"https://doi.org/10.37212/JCNOS.610132","url":null,"abstract":"The trachea has a composite structure with individual and incomplete cartilaginous rings. Deformation of trachea through surgical process and mechanical applications induces injury of laryngotracheal mucosa (Hussain et al. 2015). Results of recent studies studying the oxidative related values in larynx cancer indicated the importance of oxidative stress. Main reactive oxygen species (ROS) are superoxide radical, hydroxyl radical and singlet oxygen. Production normal level of ROS is a physiological process, because the ROS has been using for physiological functions such as killing bacteria and viruses in the body. The excessive production of ROS is scavenged by enzymatic and non-enzymatic antioxidants. 900 and 1800 MHz frequencies are used in cell phones in several countries including Turkey, although 2450 MHz has been using as Wi-Fi frequency in the countries. The non-ionize cell phone and Wi-Fi frequencies induce their hazardous effects in cells including laryngeal mucosa by excessive production of ROS. Results of recent papers indicated that the antioxidant levels such as glutathione and glutathione peroxidase were decreased in the laryngeal mucosa of animals by the cell phone and Wi-Fi exposures, but oxidative stress levels were increased by the exposures (Aynali et al. 2013). In the oral presentation, I will summarize the results of recent papers on oxidative stress and antioxidants in neurons and cells including laryngeal mucosa. In conclusion, exposure to the frequencies is accompanied by increased oxidative stress, suggesting that oxidative stress is a cause of electromagnetic radiation-induced laryngotracheal pathophysiology. For clarifying the subject, future studies need on the Wi-Fi and mobile phone frequencies-induced oxidative stress in larynx of animal and human","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46204991","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Human gut microbiota and Parkinson Disease 人类肠道微生物群与帕金森病

Journal of Cellular Neuroscience and Oxidative Stress Pub Date : 2018-08-18 DOI: 10.37212/jcnos.610152

M. Güzel

{"title":"Human gut microbiota and Parkinson Disease","authors":"M. Güzel","doi":"10.37212/jcnos.610152","DOIUrl":"https://doi.org/10.37212/jcnos.610152","url":null,"abstract":"Human gut microbiota (GM) has now been accepted as a potential modulator ofhuman biology. Although new to the world of science, GM's impaction brain and behavior has drawn great attention around the globe. Studies have now proven that GM can directly or indirectly modify brain neurochemistry via various mechanisms like neural, immune and endocrine. The intestinal microbiota influence neurodevelopment, modulate behavior, and contribute to neurological disorders. This presentation is an overview of recent findings regarding the GM -brain axis in PD (Braniste et al. 2014; Sampson et al. 2016) Parkinson disease (PD) is the second-most common neurodegenerative disorder. PD patients show alpha-synuclein deposits and neurodegeneration in the enteric nervous system as well as breakdown of the mucosal barrier, bacterial invasion, and mucosal inflammation in the colon. Alterations in GM and increased gut permeability may influence PD pathophysiology via epigenetic processes that alter αSyn regulation (Matsumoto et al. 2010). Sampson et al. (2016) suggest that GM are required for the hallmark motor and GI dysfunction in a mouse model of PD, via postnatal gut-brain signaling by microbial molecules that impact neuroinflammation and αSyn aggregation. They propose that GM regulate movement disorders and suggest that alterations in the human microbiome represent a risk factor for PD. GM do not only affect gut physiology, but there is also an intense bidirectional interaction with the brain influencing neuronal activity, behavior, as well as levels of neurotransmitter receptors, neurotrophic factors, and inflammation. Recently, gut microbiome alterations in PD subjects and a connection between GM and motoras well as non-motor symptoms have been described (Sampson et al. 2016; Parashar and Udayabanu 2017)","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47910351","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Role of melatonin on oxidative stress in traumatic brain injury 褪黑素在创伤性脑损伤氧化应激中的作用

Journal of Cellular Neuroscience and Oxidative Stress Pub Date : 2018-08-18 DOI: 10.37212/jcnos.610135

Y. Akyuva

{"title":"Role of melatonin on oxidative stress in traumatic brain injury","authors":"Y. Akyuva","doi":"10.37212/jcnos.610135","DOIUrl":"https://doi.org/10.37212/jcnos.610135","url":null,"abstract":"Oxidative stress occurs in the several physiological processes such as phagocytic activity and mitochondrial membrane functions. Oxidative stress is controlled by several enzymatic and non-enzymatic antioxidants. Traumatic brain injury is one of the most common causes of the mortalities. Secondary events occur after primary events like shearing of nerve cells and blood vessels, cause posttraumatic neurodegenerations with an increase in ROS and ROSmediated lipid peroxidation. Melatonin is a member of non-enzymatic antioxidant group. The protective effects of melatonin on traumatic brain injury have been shown in vivo and in vitro studies (Barlow et al. 2018). Also melatonin has been shown to counteract oxidative stress-induced pathophysiologic conditions like ischemia/reperfusion injury, neuronal excitotoxicity and chronic inflammation. Recently, it was reported that TBI-induced oxidative stress in experimental TBI was inhibited by the melatonin treatment (Senol and Naziroglu, 2014). In the oral presentation, I will review recent studies on traumatic brain injury in human and rodents. I concluded that the oxidative stress causes changes through activation of second messengers, which may lead to the pathology of TBI, although melatonin has protective effects on the pathology. It seems to that the exact relationship between melatonin and TBI still remain to be determined.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47193673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Dysbiosis of gut microbiota and Alzheimer’s Disease 肠道菌群失调与阿尔茨海默病

Journal of Cellular Neuroscience and Oxidative Stress Pub Date : 2018-08-18 DOI: 10.37212/jcnos.610150

O. Akpınar

{"title":"Dysbiosis of gut microbiota and Alzheimer’s Disease","authors":"O. Akpınar","doi":"10.37212/jcnos.610150","DOIUrl":"https://doi.org/10.37212/jcnos.610150","url":null,"abstract":"Alzheimer's Disease (AD) is a degenerative, chronic, progressive disease of CNS. Pathological changes that develop in the course of the disease lead to memory loss, alteration of thought, and deterioration of other brain functions. The disease progresses slowly, resulting in cell death and brain damage (Jiang 2017; Knopman 2016). Increased permeability of the intestinal and blood brain barrier due to microbial dysbosis plays a role in the pathogenesis of AD and other neurodegenerative disorders associated with aging. In addition, intestinal microbiota bacterial populations secrete amyloids and lipopolysaccharides in large quantities, which may contribute to the modulation of signaling pathways and the production of proinflammatory cytokines associated with the pathogenesis of AD (Jiang 2017). Amyloid precursor protein (APP) , which constitutes Aβ plaques and is normally secreted by intestinal bacteria, is expressed by the enteric nervous system. However, the accumulation corrupts the CNS functions. Escherichia Coli and Salmonella Enterica are some of the many bacterial strains that express and secrete APP and play a role in the pathogenesis of AD (Tse 2017). Production and clearance of Aβ in CNS is a dynamic change and some bacteria and fungi are amyloid secretions, which disrupt the dynamic balance of Aβ protein in CNS and increase the amyloid levels. This causes Aβ protein accumulation in the brain and a high risk of AD (Hill 2015).It is very important for cognitive function in serotonin, 95% of serotonin is synthesized in intestines and intestinal microorganisms play an important role in the synthesis of serotonin. There is evidence that serotonin may reduce the formation of Aβ plaques and thus reduce AD risk (Hill 2015; Jiang 2017).","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47368946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0