Journal of neurology and experimental neuroscience最新文献_第6页

Citicoline in the Treatment of Cognitive Impairment 胞糖胆碱治疗认知障碍

Journal of neurology and experimental neuroscience Pub Date : 2019-01-01 DOI: 10.17756/JNEN.2019-047

J. Secades

引用次数: 20

Patients with Sensory Symptoms of Acral Paresthesia: Routine Laboratory Findings in Neuromuscular Consultation 肢端感觉异常症状患者:神经肌肉会诊的常规实验室结果

Journal of neurology and experimental neuroscience Pub Date : 2019-01-01 DOI: 10.17756/jnen.2019-053

J. Luo, F. Bumanlag, N. Dun

引用次数: 4

Urokinase-type Plasminogen Activator Induces Neurorepair in the Ischemic Brain. 尿激酶型纤溶酶原激活剂诱导缺血性脑的神经修复。

Journal of neurology and experimental neuroscience Pub Date : 2018-01-01 Epub Date: 2018-09-26 DOI: 10.17756/jnen.2018-039

Paola Merino, Manuel Yepes

{"title":"Urokinase-type Plasminogen Activator Induces Neurorepair in the Ischemic Brain.","authors":"Paola Merino, Manuel Yepes","doi":"10.17756/jnen.2018-039","DOIUrl":"https://doi.org/10.17756/jnen.2018-039","url":null,"abstract":"Urokinase-type plasminogen activator (uPA) is a serine proteinase that upon binding to its receptor (uPAR) catalyzes the conversion of plasminogen into plasmin on the cell surface. Recent studies indicate that neurons but not astrocytes release uPA during the recovery phase from an ischemic injury, and that binding of uPA to uPAR promotes neurorepair in the ischemic brain by a mechanism that does not require plasmin generation. A combined approach of in vitro and in vivo studies has shown that uPA binding to uPAR induces the reorganization of the actin cytoskeleton in dendritic spines and axons that have suffered an ischemic injury. Furthermore, recent data indicate that uPA-uPAR binding induces astrocytic activation and a crosstalk between activated astrocytes and the injured neuron that triggers a sequence of biochemical events that promote the repair of synapses injured by the ischemic insult. The translational relevance of these observations is noteworthy because following its intravenous administrations recombinant uPA (ruPA) reaches the ischemic tissue, thus raising the question of whether treatment with ruPA is an effective therapeutic strategy to promote neurorepair functional recovery among ischemic stroke survivors.","PeriodicalId":91755,"journal":{"name":"Journal of neurology and experimental neuroscience","volume":"4 2","pages":"24-29"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6225521/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36665746","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}

引用次数: 12

GSK249320, A Monoclonal Antibody Against the Axon Outgrowth Inhibition Molecule Myelin-Associated Glycoprotein, Improves Outcome of Rodents with Experimental Stroke 抗轴突生长抑制分子髓鞘相关糖蛋白的单克隆抗体GSK249320改善实验性脑卒中啮齿动物的预后

Journal of neurology and experimental neuroscience Pub Date : 2016-11-21 DOI: 10.17756/JNEN.2016-014

D. Cash, A. Easton, M. Mesquita, J. Beech, S. Williams, Andrew Lloyd, E. Irving, S. Cramer

{"title":"GSK249320, A Monoclonal Antibody Against the Axon Outgrowth Inhibition Molecule Myelin-Associated Glycoprotein, Improves Outcome of Rodents with Experimental Stroke","authors":"D. Cash, A. Easton, M. Mesquita, J. Beech, S. Williams, Andrew Lloyd, E. Irving, S. Cramer","doi":"10.17756/JNEN.2016-014","DOIUrl":"https://doi.org/10.17756/JNEN.2016-014","url":null,"abstract":"Myelin-associated glycoprotein (MAG) is an inhibitor of axon growth. MAG levels increase after stroke. GSK249320 is a monoclonal antibody that neutralizes MAG-mediated inhibition and so may promote axon outgrowth and improve post-stroke outcomes. The current study tested the hypothesis that GSK249320 initiated 24 hours or 7 days after experimental stroke improves behavioural outcomes. Rats with right middle cerebral artery occlusion for 90 minutes were randomized to receive 6 weeks of intravenous (a) GSK249320 starting 24 hours post-stroke, (b) GSK249320 starting 7 days post-stroke, or (c) vehicle. Behavioral testing was performed over 7 weeks. Serial MRI demonstrated no differences in infarct volume across groups. Animals treated with GSK249320 24 hours post-stroke showed larger increases in Neuroscore (time X group, p = 0.0008) and staircase test (main effect of group, p = 0.0214) as compared to controls, but animals treated 7 days post-stroke showed no significant behavioral benefit. No significant results were found for the sticky tape or cylinder tests. A separate set of animals with experimental stroke received a single intravenous dose of GSK249320 or vehicle at 1 hour, 24 hours, 48 hours or 1 week post-stroke, and immunohistochemistry methods were used to measure GSK249320 distribution; GSK249320 was found in the ipsilesional hemisphere only, the extent of which increased with later times of injection. These data suggest that intravenous GSK249320 penetrates the lesion site and is associated with a small effect on functional outcomes when initiated 24 hours post-stroke and so support the translational potential of this monoclonal antibody as a restorative therapy for patients with stroke.","PeriodicalId":91755,"journal":{"name":"Journal of neurology and experimental neuroscience","volume":"2 1","pages":"28 - 33"},"PeriodicalIF":0.0,"publicationDate":"2016-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67647276","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: 12

Neurophysiological and Morphometric Characteristics of Restless Legs Syndrome in Parkinson’s Disease 帕金森病不宁腿综合征的神经生理学和形态计量学特征

Journal of neurology and experimental neuroscience Pub Date : 1900-01-01 DOI: 10.17756/jnen.2019-s1-003

O. A. Alenikova, Nikita V Alenikov, S. Likhachev

引用次数: 0