نمایش مختصر رکورد

dc.contributor.authorCerina, Men_US
dc.contributor.authorNarayanan, Ven_US
dc.contributor.authorDelank, Aen_US
dc.contributor.authorGallus, Men_US
dc.contributor.authorDik, Aen_US
dc.contributor.authorHerrmann, A.Men_US
dc.contributor.authorGöbel, Ken_US
dc.contributor.authorMeuth, Pen_US
dc.contributor.authorPape, H.-Cen_US
dc.contributor.authorBudde, Ten_US
dc.contributor.authorMeuth, S.Gen_US
dc.date.accessioned1399-08-22T00:36:35Zfa_IR
dc.date.accessioned2020-11-12T00:36:35Z
dc.date.available1399-08-22T00:36:35Zfa_IR
dc.date.available2020-11-12T00:36:35Z
dc.date.issued2017-04-01en_US
dc.date.issued1396-01-12fa_IR
dc.identifier.citation(1396). مجله علوم اعصاب شفای خاتم, 5(2), 12-12.fa_IR
dc.identifier.issn2322-1887
dc.identifier.issn2345-4814
dc.identifier.urihttp://shefayekhatam.ir/article-1-1166-en.html
dc.identifier.urihttps://iranjournals.nlai.ir/handle/123456789/499691
dc.description.abstractMultiple Sclerosis (MS) is a complex disease resulting from the occurrence of intermingled episodes of neuro-inflammation and degeneration. The temporal and spatial patterns in which these events occur are not well understood as well as the molecular substrates underlying it. Myelin loss and gain, as well as axonal damage are considered crucial events influencing the course of the disease but their cause/effect dependency remains unclear. Numerous recent evidence showed impaired cognitive behaviors both in MS patients and animal models, which would support a profound involvement of neurons in mediating such effects, along to the long-known MS hallmarks like locomotor deficits and slow axonal conductance, attributed mainly to myelin loss. In order to investigate the role of neurons and their functionality in the pathophysiology on MS we took advantage of different animal models of neuro-inflammation and general de- and remyelination, namely the experimental autoimmune encephalitis (EAE) and the cuprizone model, respectively. For both animals we could observe the occurrence of different cognitive impairments including loss of short and long term memory and of high functional cortical abilities. In both animals models we could associate these symptoms to an altered neuronal network excitability and therefore, we pursued pharmacological modulation in vitro and in vivo in order to verify this finding by identifying potential molecular players. Therefore, by using different novel or established compounds we tried to identify new drugable targets and new therapeutic time windows for intervention.en_US
dc.format.extent208
dc.format.mimetypeapplication/pdf
dc.languageEnglish
dc.language.isoen_US
dc.publisherتهران مرکز تحقیقات علوم اعصاب شفاءfa_IR
dc.relation.ispartofمجله علوم اعصاب شفای خاتمfa_IR
dc.relation.ispartofThe Neuroscience Journal of Shefaye Khatamen_US
dc.subjectMultiple sclerosisen_US
dc.subjectAnimal modelsen_US
dc.subjectLocomotor deficitsen_US
dc.subjectBasic research in Neuroscienceen_US
dc.titleO 12: The Pathophysiological Hallmarks of MS Beyond the Blood Brain Barrier: Myelination and Neuronal Network Interactionsen_US
dc.typeTexten_US
dc.typeReview --- Open Access, CC-BY-NCen_US
dc.contributor.departmentUniversitätsklinikum Münster, Institut Für Translationale Neurologie, Münster, Germanyen_US
dc.contributor.departmentUniversitätsklinikum Münster, Institut Für Translationale Neurologie, Münster, Germanyen_US
dc.contributor.departmentUniversitätsklinikum Münster, Institut Für Translationale Neurologie, Münster, Germanyen_US
dc.contributor.departmentUniversitätsklinikum Münster, Institut Für Translationale Neurologie, Münster, Germanyen_US
dc.contributor.departmentUniversitätsklinikum Münster, Institut Für Translationale Neurologie, Münster, Germanyen_US
dc.contributor.departmentUniversitätsklinikum Münster, Institut Für Translationale Neurologie, Münster, Germanyen_US
dc.contributor.departmentUniversitätsklinikum Münster, Institut Für Translationale Neurologie, Münster, Germanyen_US
dc.contributor.departmentUniversitätsklinikum Münster, Institut Für Translationale Neurologie, Münster, Germanyen_US
dc.contributor.departmentUniversitätsklinikum Münster, Institut Für Translationale Neurologie, Münster, Germanyen_US
dc.contributor.departmentUniversitätsklinikum Münster, Institut Für Translationale Neurologie, Münster, Germanyen_US
dc.contributor.departmentUniversitätsklinikum Münster, Institut Für Translationale Neurologie, Münster, Germanyen_US
dc.citation.volume5
dc.citation.issue2
dc.citation.spage12
dc.citation.epage12


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