Advances in Neuroimmune Biology最新文献_第8页

Immunosuppressive Activity of Adult Marrow Mesenchymal Stromal Cells on Innate Immune Cells in the Central Nervous System 成人骨髓间充质基质细胞对中枢神经系统先天免疫细胞的免疫抑制作用

Advances in Neuroimmune Biology Pub Date : 2013-01-01 DOI: 10.3233/NIB-130064

M. Dao, J. Nolta, C. Case

引用次数: 1

Neural Dysfunction in Chronic Fatigue Syndrome 慢性疲劳综合征的神经功能障碍

Advances in Neuroimmune Biology Pub Date : 2013-01-01 DOI: 10.3233/NIB-130065

Masaaki Tanaka, Akira Ishii, Yasuyoshi Watanabe

{"title":"Neural Dysfunction in Chronic Fatigue Syndrome","authors":"Masaaki Tanaka, Akira Ishii, Yasuyoshi Watanabe","doi":"10.3233/NIB-130065","DOIUrl":"https://doi.org/10.3233/NIB-130065","url":null,"abstract":"Chronic fatigue syndrome (CFS) is characterized by a profound, disabling, and unexplained sensation of fatigue lasting an unexplained severe fatigue which lasts for at least 6 months with a combination of various symptoms, and it impairs patients' ability to live their days normally. Patients with CFS complain of neuropsychological symptoms, including cognitive impairment (thinking difficulties, decreased alertness, and impaired memory and concentration), chronic widespread pain (muscle pain, pain in multiple joints, headaches, and sore throat), and depressive symptoms. In addition, many studies have shown abnormalities in the central nervous system (CNS) in patients with CFS. These findings suggest that the CNS is primarily involved in the pathophysiology of CFS. Here, we review data primarily from behavioral, electrophysiological, and neuroimaging experiments related to neural dysfunction in CFS. Dysfunction of a facilitation system and central sensitization and classical conditioning of an inhibition system in the CNS seem to play pivotal roles in the pathophysiology of CFS. We also propose a treatment strategy for CFS on the basis of these suggested underlying neural mechanisms.","PeriodicalId":38645,"journal":{"name":"Advances in Neuroimmune Biology","volume":"9 1","pages":"291-300"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3233/NIB-130065","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70144466","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

Microglial Activation in Immunologically Induced Fatigue 免疫诱导疲劳中的小胶质细胞激活

Advances in Neuroimmune Biology Pub Date : 2013-01-01 DOI: 10.3233/NIB-130075

M. Ifuku, Shamim Hossain, T. Katafuchi

引用次数: 0

Dietary Acetate Supplementation Attenuates Neuroinflammation 膳食中补充醋酸盐可减轻神经炎症

Advances in Neuroimmune Biology Pub Date : 2013-01-01 DOI: 10.3233/NIB-130060

Mahmoud L. Soliman, T. A. Rosenberger

{"title":"Dietary Acetate Supplementation Attenuates Neuroinflammation","authors":"Mahmoud L. Soliman, T. A. Rosenberger","doi":"10.3233/NIB-130060","DOIUrl":"https://doi.org/10.3233/NIB-130060","url":null,"abstract":"The innate immune response maintains a vital role in the health of the central nervous system. Within the central nervous system the innate immune response is initiated following the binding of antigen to microglia that activates inflammatory cascades within the cell, recruits other microglial cells to the sight of action, and induces reactive astrogliosis of neighboring astrocytes. Under normal circumstance, once the antigen is cleared both the activated microglia and reactive astrocytes return to their quiescent or ramified states. With many neurological diseases and injury, neuroinflammatory cascades become tonically activated resulting in sustained neuroglia activation that can result in the induction, and/or progression of neurological injury. Because neuroinflammation is a key pathological element found in many neurological disorders it is believed that reducing inflammatory events in the brain can reduce injury and slow disease progression. In this regard, acetate supplementation by increasing the intracellular concentration of the metabolically active intermediate acetyl-CoA imparts both anti-inflammatory and neuroprotective properties. In this review, we summarize the current state of knowledge concerning the metabolism of acetate within the central nervous system and explore potential mechanisms of action by which acetate reduces neuroglial activation and neuroinflammatory signaling.","PeriodicalId":38645,"journal":{"name":"Advances in Neuroimmune Biology","volume":"4 1","pages":"125-140"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3233/NIB-130060","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70144722","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: 1

Autonomic Dysfunction in Chronic Fatigue Syndrome 慢性疲劳综合征的自主神经功能障碍

Advances in Neuroimmune Biology Pub Date : 2013-01-01 DOI: 10.3233/NIB-130072

K. Yamaguti, Seiki Tajima, H. Kuratsune

{"title":"Autonomic Dysfunction in Chronic Fatigue Syndrome","authors":"K. Yamaguti, Seiki Tajima, H. Kuratsune","doi":"10.3233/NIB-130072","DOIUrl":"https://doi.org/10.3233/NIB-130072","url":null,"abstract":"Symptoms of autonomic dysfunction are one of the characteristic features of the clinical condition known as chronic fatigue syndrome (CFS). In this study we examined the autonomic nerve functions in 1,099 patients with CFS and in 361 normal healthy controls. The autonomic nerve functions were studied in terms of heart rate variability and spectral analysis, and by using the maximal Lyapunov exponent (MLE) and chaotic analysis. The heart rate variability analysis revealed that both the logarithmic low-frequency power (Log LF) and logarithmic high-frequency power (Log HF) were reduced significantly with age in healthy subjects (p < 0.005). When we compared these parameters between the CFS patients and healthy controls according to age groups, there was no significant difference in Log LF between CFS and control except in the case of the 40's age group. However, Log HF decreased significantly in moderate and severe fatigue CFS groups in all age groups. All of the severe fatigue CFS age groups had a significant increase in the ratio of Log LF/HF as compared with that of the healthy controls. When we studied the change in these power values during sleep as compared with that during awake time, the HF power rose 3.03-fold in the controls and 1.86-fold in the CFS group during sleep as compared with that during the awake time; and this difference in fold increase during sleep between the CFS and control groups was significant (p < 0.05). Furthermore, the MLE for both the moderate and severe fatigue CFS groups was decreased significantly as compared with that of the healthy control group (p < 0.01). It is well known that autonomic nervous function differs greatly in individuals, but our present large research study indicates that there is no doubt that parasympathetic nervous dysfunction is involved in the pathophysiology of CFS patients with severe fatigue. We incorporated the evaluation of autonomic function into the Japanese CFS diagnostic criteria in 2012, because this evaluation might be a useful objective diagnostic tool for CFS.","PeriodicalId":38645,"journal":{"name":"Advances in Neuroimmune Biology","volume":"4 1","pages":"281-289"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3233/NIB-130072","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70144814","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: 11

Ghrelin: A GH-Releasing, Appetite-Regulating Gastric Hormone 胃饥饿素:一种释放gh、调节食欲的胃激素

Advances in Neuroimmune Biology Pub Date : 2013-01-01 DOI: 10.3233/NIB-130051

J. D. Michele, F. Rotondo, K. Kovacs, A. Ieva, L. Syro, E. Latta, M. Cusimano

引用次数: 0

LRRK-2 as a Key Molecule Bridging Inflammation to Parkinson's Disease LRRK-2是连接炎症与帕金森病的关键分子

Advances in Neuroimmune Biology Pub Date : 2013-01-01 DOI: 10.3233/NIB-130067

V. Roca, M. Puntel

引用次数: 0

Dysfunction in the Hypothalamo-Hypophyseal System under Chronic Stress and Fatigue 慢性应激和疲劳下下丘脑-垂体系统的功能障碍

Advances in Neuroimmune Biology Pub Date : 2013-01-01 DOI: 10.3233/NIB-130070

T. Ogawa, H. Konishi, H. Kiyama

引用次数: 0

MicroRNAs as Diagnostic and Therapeutic Targets in Multiple Sclerosis MicroRNAs作为多发性硬化的诊断和治疗靶点

Advances in Neuroimmune Biology Pub Date : 2013-01-01 DOI: 10.3233/NIB-130053

M. P. Kakhki, Abbas Nikravesh, P. Kokhaei

引用次数: 1

Microglia and Glutamate 小胶质细胞和谷氨酸

Advances in Neuroimmune Biology Pub Date : 2013-01-01 DOI: 10.3233/NIB-130057

H. Takeuchi

{"title":"Microglia and Glutamate","authors":"H. Takeuchi","doi":"10.3233/NIB-130057","DOIUrl":"https://doi.org/10.3233/NIB-130057","url":null,"abstract":"Accumulation of activated microglia around degenerative neurons is a common pathological observation in a variety of neurologic disorders. Activated microglia release a large amount of glutamate that induces neurodegeneration in numerous neurologic diseases such as ischemia, inflammation, epilepsy, and neurodegenerative diseases. Although both blockade of glutamate receptors and inhibition of microglial activation are the therapeutic candidates for activated microglia-mediated neurodegenerative diseases, clinical trials have been failed because of adverse effects presumably stemming from disrupted physiological glutamate signaling and suppressed neuroprotective microglial functions. Recent studies revealed that activated microglia specifically produce glutamate using glutaminase and release glutamate via cell-surface gap junction hemichannels. Blockade of microglial hemichannel successfully suppressed disease progression in animal models of brain ischemia, chronic neuropathic pain, multiple sclerosis, amyotrophic lateral sclerosis, and Alzheimer's disease. Therefore, hemichannel blockers may offer a promising therapy for various neurologic disorders without causing the above-mentioned adverse effects.","PeriodicalId":38645,"journal":{"name":"Advances in Neuroimmune Biology","volume":"4 1","pages":"77-83"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3233/NIB-130057","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70143999","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: 2