Gelişmiş Arama

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dc.contributor.authorAlyu, Feyza
dc.contributor.authorDikmen, Miriş
dc.date.accessioned2019-10-19T14:03:14Z
dc.date.available2019-10-19T14:03:14Z
dc.date.issued2017
dc.identifier.issn1601-5215
dc.identifier.urihttps://dx.doi.org/10.1017/neu.2016.47
dc.identifier.urihttps://hdl.handle.net/11421/12541
dc.descriptionWOS: 000393657200001en_US
dc.descriptionPubMed ID: 27692004en_US
dc.description.abstractObjective Epilepsy is a chronic neurological disease characterised with seizures. The aetiology of the most generalised epilepsies cannot be explicitly determined and the seizures are pronounced to be genetically determined by disturbances of receptors in central nervous system. Besides, neurotransmitter distributions or other metabolic problems are supposed to involve in epileptogenesis. Lack of adequate data about pharmacological agents that have antiepileptogenic effects point to need of research on this field. Thus, in this review, inflammatory aspects of epileptogenesis has been focussed via considering several concepts like role of immune system, blood-brain barrier and antibody involvement in epileptogenesis. Methods We conducted an evidence-based review of the literatures in order to evaluate the possible participation of inflammatory processes to epileptogenesis and also, promising agents which are effective to these processes. We searched PubMed database up to November 2015 with no date restrictions. Results In the present review, 163 appropriate articles were included. Obtained data suggests that inflammatory processes participate to epileptogenesis in several ways like affecting fibroblast growth factor-2 and tropomyosin receptor kinase B signalling pathways, detrimental proinflammatory pathways [such as the interleukin-1 beta (IL-1)-interleukin-1 receptor type 1 (IL-1R1) system], mammalian target of rapamycin pathway, microglial activities, release of glial inflammatory proteins (such as macrophage inflammatory protein, interleukin 6, C-C motif ligand 2 and IL-1), adhesion molecules that are suggested to function in signalling pathways between neurons and microglia and also linkage between these molecules and proinflammatory cytokines. Conclusion The literature research indicated that inflammation is a part of epileptogenesis. For this reason, further studies are necessary for assessing agents that will be effective in clinical use for therapeutic treatment of epileptogenesis.en_US
dc.language.isoengen_US
dc.publisherCambridge University Pressen_US
dc.relation.isversionof10.1017/neu.2016.47en_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectEpilepsyen_US
dc.subjectEpileptogenesisen_US
dc.subjectInflammationen_US
dc.titleInflammatory aspects of epileptogenesis: contribution of molecular inflammatory mechanismsen_US
dc.typereviewen_US
dc.relation.journalActa Neuropsychiatricaen_US
dc.contributor.departmentAnadolu Üniversitesi, Eczacılık Fakültesi, Eczacılık Temel Bilimleri Anabilim Dalıen_US
dc.identifier.volume29en_US
dc.identifier.issue1en_US
dc.identifier.startpage1en_US
dc.identifier.endpage16en_US
dc.relation.publicationcategoryDiğeren_US
dc.contributor.institutionauthorDikmen, Miriş


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