Vascular cognitive impairment is a process which is more frequent in patients with cardiovascular risk factors. The etiology of this kind of impairment could be related to different types of cerebrovascular disorders, given that silent cerebral infarctions or microinfarcts, correlated with small vessel disease, are one of the principal etiologies. Microinfarcts, associated with small vessel diseases, should be considered one of the possible causes of clinical suspicion in patients with cardiovascular risk factors who are asking for help for cognitive complaints. Among the proposed treatments for cognitive impairment there is citicoline. This is an updated review of the possible use of citicoline in the treatment of cognitive impairment.
{"title":"Citicoline in the Treatment of Cognitive Impairment","authors":"J. Secades","doi":"10.17756/JNEN.2019-047","DOIUrl":"https://doi.org/10.17756/JNEN.2019-047","url":null,"abstract":"Vascular cognitive impairment is a process which is more frequent in patients with cardiovascular risk factors. The etiology of this kind of impairment could be related to different types of cerebrovascular disorders, given that silent cerebral infarctions or microinfarcts, correlated with small vessel disease, are one of the principal etiologies. Microinfarcts, associated with small vessel diseases, should be considered one of the possible causes of clinical suspicion in patients with cardiovascular risk factors who are asking for help for cognitive complaints. Among the proposed treatments for cognitive impairment there is citicoline. This is an updated review of the possible use of citicoline in the treatment of cognitive impairment.","PeriodicalId":91755,"journal":{"name":"Journal of neurology and experimental neuroscience","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67648081","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}
{"title":"Patients with Sensory Symptoms of Acral Paresthesia: Routine Laboratory Findings in Neuromuscular Consultation","authors":"J. Luo, F. Bumanlag, N. Dun","doi":"10.17756/jnen.2019-053","DOIUrl":"https://doi.org/10.17756/jnen.2019-053","url":null,"abstract":"","PeriodicalId":91755,"journal":{"name":"Journal of neurology and experimental neuroscience","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67648177","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 : 2018-01-01Epub Date: 2018-09-26DOI: 10.17756/jnen.2018-039
Paola Merino, Manuel Yepes
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.
{"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":"<p><p>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 <i>in vitro</i> and <i>in vivo</i> 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.</p>","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}
D. Cash, A. Easton, M. Mesquita, J. Beech, S. Williams, Andrew Lloyd, E. Irving, S. Cramer
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.
{"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}
Pub Date : 1900-01-01DOI: 10.17756/jnen.2019-s1-003
O. A. Alenikova, Nikita V Alenikov, S. Likhachev
{"title":"Neurophysiological and Morphometric Characteristics of Restless Legs Syndrome in Parkinson’s Disease","authors":"O. A. Alenikova, Nikita V Alenikov, S. Likhachev","doi":"10.17756/jnen.2019-s1-003","DOIUrl":"https://doi.org/10.17756/jnen.2019-s1-003","url":null,"abstract":"","PeriodicalId":91755,"journal":{"name":"Journal of neurology and experimental neuroscience","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67648674","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}
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