Pub Date : 2021-07-17DOI: 10.46439/neuroscience.2.009
{"title":"Propriospinal neurons involved in coordination of the bladder and urethra","authors":"","doi":"10.46439/neuroscience.2.009","DOIUrl":"https://doi.org/10.46439/neuroscience.2.009","url":null,"abstract":"","PeriodicalId":75148,"journal":{"name":"The neuroscience chronicles","volume":"55 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83838652","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}
Pub Date : 2021-07-17DOI: 10.46439/neuroscience.2.007
Puigoriol-Illamola, Griñán-Ferré
In recent years, stress and stress-coping mechanisms constitute a growing public healthcare issue concerning modern society. Experiencing stress engenders a great complex mechanism named stress response, which consists of a rapid release of catecholamines by the sympathetic nervous system, followed by a slower response in which hormones, mainly glucocorticoids (GCs), are synthesized and released to the bloodstream. Once the stressful stimulus is perceived, the hypothalamus
{"title":"Inhibition of 11β-HSD1, a key enzyme in the stress management, improves cognition by RL-118 drug treatment","authors":"Puigoriol-Illamola, Griñán-Ferré","doi":"10.46439/neuroscience.2.007","DOIUrl":"https://doi.org/10.46439/neuroscience.2.007","url":null,"abstract":"In recent years, stress and stress-coping mechanisms constitute a growing public healthcare issue concerning modern society. Experiencing stress engenders a great complex mechanism named stress response, which consists of a rapid release of catecholamines by the sympathetic nervous system, followed by a slower response in which hormones, mainly glucocorticoids (GCs), are synthesized and released to the bloodstream. Once the stressful stimulus is perceived, the hypothalamus","PeriodicalId":75148,"journal":{"name":"The neuroscience chronicles","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83051113","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}
Pub Date : 2021-01-01DOI: 10.46439/neuroscience.2.012
Agnes Badu-Mensah, Xiufang Guo, James J Hickman
Aside its function in locomotion, posture maintenance and respiration, the human skeletal muscle (hSKM) is reported to be a critical metabolic regulator [1]. The hSKM is acknowledged as the primary site of glucose metabolism and storage [1]. Additionally, it serves as a reservoir for amino acids [1,2]. In recently times, the hSKM has also been described as an endocrine organ. It is known to secrete a plethora of myokines that systemically affect other organs including the liver, pancreas, and immune system among others [3,4]. Proper function of the hSKM is therefore critical for maintaining whole body metabolic homeostasis. As such, perturbations in skeletal muscle resulting in metabolic and functional changes has deleterious consequences on the overall health of an organism. Unsurprisingly, muscle health decline is associated with poor disease prognosis in numerous conditions [2]. Thus, paying attention to muscle health may be pertinent to improving disease outcomes and overall wellbeing of an organism.
{"title":"ALS Skeletal Muscle: Victim or Culprit.","authors":"Agnes Badu-Mensah, Xiufang Guo, James J Hickman","doi":"10.46439/neuroscience.2.012","DOIUrl":"https://doi.org/10.46439/neuroscience.2.012","url":null,"abstract":"Aside its function in locomotion, posture maintenance and respiration, the human skeletal muscle (hSKM) is reported to be a critical metabolic regulator [1]. The hSKM is acknowledged as the primary site of glucose metabolism and storage [1]. Additionally, it serves as a reservoir for amino acids [1,2]. In recently times, the hSKM has also been described as an endocrine organ. It is known to secrete a plethora of myokines that systemically affect other organs including the liver, pancreas, and immune system among others [3,4]. Proper function of the hSKM is therefore critical for maintaining whole body metabolic homeostasis. As such, perturbations in skeletal muscle resulting in metabolic and functional changes has deleterious consequences on the overall health of an organism. Unsurprisingly, muscle health decline is associated with poor disease prognosis in numerous conditions [2]. Thus, paying attention to muscle health may be pertinent to improving disease outcomes and overall wellbeing of an organism.","PeriodicalId":75148,"journal":{"name":"The neuroscience chronicles","volume":"2 2","pages":"31-33"},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/99/ff/nihms-1770505.PMC8793963.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39873146","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-12-31DOI: 10.46439/neuroscience.1.001
Rudrarup Bhattacharjee, Dr. Amarendranath Choudhury
While much of research progress has been achieved in last century on Alzheimer’s Disease (AD), the conclusive therapy for the same is still unachieved. Several lines of therapeutic regimes have been introduced, which basically act on slowing down the disease progression. However, adverse side effects on lifelong use of such synthetic drugs are also inevitable. Rationale of such realization has attracted researchers to find alternative medicine for AD therapeutics. Natural products have shown promising response in this regard. Among handful of herbal products, Ginseng is notable and capable of recapitulating the equivalent functional attributes like other synthetic drugs available, with no side effects. In the present communication, based on available literature and reported data, we will discuss various aspects of Ginseng attribution as a potential alternative therapeutic approach for AD and whether it may serve as a novel pathway to treat AD.
{"title":"Role of Ginseng in therapeutic management of Alzheimer’s Disease","authors":"Rudrarup Bhattacharjee, Dr. Amarendranath Choudhury","doi":"10.46439/neuroscience.1.001","DOIUrl":"https://doi.org/10.46439/neuroscience.1.001","url":null,"abstract":"While much of research progress has been achieved in last century on Alzheimer’s Disease (AD), the conclusive therapy for the same is still unachieved. Several lines of therapeutic regimes have been introduced, which basically act on slowing down the disease progression. However, adverse side effects on lifelong use of such synthetic drugs are also inevitable. Rationale of such realization has attracted researchers to find alternative medicine for AD therapeutics. Natural products have shown promising response in this regard. Among handful of herbal products, Ginseng is notable and capable of recapitulating the equivalent functional attributes like other synthetic drugs available, with no side effects. In the present communication, based on available literature and reported data, we will discuss various aspects of Ginseng attribution as a potential alternative therapeutic approach for AD and whether it may serve as a novel pathway to treat AD.","PeriodicalId":75148,"journal":{"name":"The neuroscience chronicles","volume":"46 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90636841","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}
Pub Date : 2020-12-31DOI: 10.46439/neuroscience.1.002
S. Bittmann, A. Weissenstein, G. Villalon, E. Moschüring-Alieva, E. Luchter
In the nightmare of the coronavirus pandemic that is spreading around the world, parents could take comfort in one thing early reports that the virus mysteriously spares children, even though this often leads to critical illness in older people. An article published in the Journal “Pediatrics”, based on 2,143 young people in China, provides the most comprehensive evidence of the spread of the virus among children, and there is bad news and good news [1]. The study confirms that coronavirus infections in children are generally less severe, with more than 90 percent having mild to moderate disease or even being asymptomatic and have more transmitter function for elder people.
{"title":"Association of COVID-19 coronavirus and Kawasaki syndrome like features in 1-5 years old children","authors":"S. Bittmann, A. Weissenstein, G. Villalon, E. Moschüring-Alieva, E. Luchter","doi":"10.46439/neuroscience.1.002","DOIUrl":"https://doi.org/10.46439/neuroscience.1.002","url":null,"abstract":"In the nightmare of the coronavirus pandemic that is spreading around the world, parents could take comfort in one thing early reports that the virus mysteriously spares children, even though this often leads to critical illness in older people. An article published in the Journal “Pediatrics”, based on 2,143 young people in China, provides the most comprehensive evidence of the spread of the virus among children, and there is bad news and good news [1]. The study confirms that coronavirus infections in children are generally less severe, with more than 90 percent having mild to moderate disease or even being asymptomatic and have more transmitter function for elder people.","PeriodicalId":75148,"journal":{"name":"The neuroscience chronicles","volume":"30 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77993407","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}
Pub Date : 2020-01-01DOI: 10.46439/neuroscience.1.004
Neelima B Chauhan
Alzheimer's disease (AD) is a global health crisis currently afflicting ~6 million Americans (and ~40 million people worldwide). By the middle of the century, these numbers will stagger by ~16 million Americans (and ~152 million people worldwide) suffering from AD, if breakthrough disease-modifying treatments are not discovered. Currently, there are no treatments to prevent, halt or cure the disease. Multiple independent studies on brain gene expression patterns have indicated that in AD about 1/3rd of the genes are upregulated while the rest 2/3rd of the genes are downregulated. In that regard, AD therapeutics focused on antagomiR-mediated silencing of"upregulated"microRNAs (miRs) may be more feasible since upregulated miRs in AD continue to increase with the disease progression, as opposed to agomiR-mediated overexpression of down-regulated miRs with unpredictable reduced presence and relative short-life of 1-3h under pathological conditions in AD brain. Studies reported thus far indicate that most of the upregulated pathogenic genes in AD are regulated by pro-inflammatory microRNAs (miRs). Given the precedence of chronic neuroinflammation in triggering AD-like neurodegeneration and multifactorial nature of AD, silencing inflammation-specific micro-RNAs using antisense-microRNAs may be an effective adjuvant therapeutic strategy to prevent, halt or cure AD.
阿尔茨海默病(AD)是一场全球性的健康危机,目前困扰着约 600 万美国人(全球约 4000 万人)。到本世纪中叶,如果没有突破性的改变疾病的治疗方法,这一数字将激增到约 1600 万美国人(全球约 1.52 亿人)患有阿尔茨海默病。目前,还没有任何治疗方法可以预防、阻止或治愈这种疾病。多项关于大脑基因表达模式的独立研究表明,在注意力缺失症中,约有 1/3 的基因上调,而其余 2/3 的基因下调。在这方面,由于在 AD 中,上调的 miRs 会随着疾病的发展而不断增加,因此,与 agomiR 介导的下调 miRs 的过度表达相比,AD 的治疗方法可能更加可行,因为在 AD 大脑的病理条件下,下调的 miRs 的存在减少且寿命相对较短,仅为 1-3 小时。迄今为止的研究表明,AD 中大多数上调的致病基因都是由促炎性微RNA(miRs)调控的。鉴于慢性神经炎症是诱发 AD 类神经变性的先决条件,而且 AD 具有多因素性质,因此使用反义 microRNAs 沉默炎症特异性 microRNAs 可能是预防、阻止或治愈 AD 的有效辅助治疗策略。
{"title":"MicroRNA silencing: A promising therapy for Alzheimer's disease.","authors":"Neelima B Chauhan","doi":"10.46439/neuroscience.1.004","DOIUrl":"10.46439/neuroscience.1.004","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a global health crisis currently afflicting ~6 million Americans (and ~40 million people worldwide). By the middle of the century, these numbers will stagger by ~16 million Americans (and ~152 million people worldwide) suffering from AD, if breakthrough disease-modifying treatments are not discovered. Currently, there are no treatments to prevent, halt or cure the disease. Multiple independent studies on brain gene expression patterns have indicated that in AD about 1/3<sup>rd</sup> of the genes are upregulated while the rest 2/3<sup>rd</sup> of the genes are downregulated. In that regard, AD therapeutics focused on antagomiR-mediated silencing of\"upregulated\"microRNAs (miRs) may be more feasible since upregulated miRs in AD continue to increase with the disease progression, as opposed to agomiR-mediated overexpression of down-regulated miRs with unpredictable reduced presence and relative short-life of 1-3h under pathological conditions in AD brain. Studies reported thus far indicate that most of the upregulated pathogenic genes in AD are regulated by pro-inflammatory microRNAs (miRs). Given the precedence of chronic neuroinflammation in triggering AD-like neurodegeneration and multifactorial nature of AD, silencing inflammation-specific micro-RNAs using antisense-microRNAs may be an effective adjuvant therapeutic strategy to prevent, halt or cure AD.</p>","PeriodicalId":75148,"journal":{"name":"The neuroscience chronicles","volume":"1 1","pages":"11-15"},"PeriodicalIF":0.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9389881/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40432126","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}