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dc.contributor.authorMecha, Miriames_ES
dc.contributor.authorYanguas-Casás, Nataliaes_ES
dc.contributor.authorFeliú, Anaes_ES
dc.contributor.authorMestre, Leyrees_ES
dc.contributor.authorCarrillo-Salinas, F. J.es_ES
dc.contributor.authorAzcoitia, I.es_ES
dc.contributor.authorYong, Y. W.es_ES
dc.contributor.authorGuaza, Carmenes_ES
dc.date.accessioned2019-06-03T12:55:29Z-
dc.date.available2019-06-03T12:55:29Z-
dc.date.issued2019-03-
dc.identifier.citationBrain, Behavior, and Immunity 77: 110-126 (2019)es_ES
dc.identifier.issn0889-1591-
dc.identifier.urihttp://hdl.handle.net/10261/183188-
dc.description.abstractRemyelination is an endogenous process by which functional recovery of damaged neurons is achieved by reinstating the myelin sheath around axons. Remyelination has been documented in multiple sclerosis (MS) lesions and experimental models, although it is often incomplete or fails to affect the integrity of the axon, thereby leading to progressive disability. Microglia play a crucial role in the clearance of the myelin debris produced by demyelination and in inflammation-dependent OPC activation, two processes necessary for remyelination to occur. We show here that following corpus callosum demyelination in the TMEV-IDD viral murine model of MS, there is spontaneous and partial remyelination that involves a temporal discordance between OPC mobilization and microglia activation. Pharmacological treatment with the endocannabinoid 2-AG enhances the clearance of myelin debris by microglia and OPC differentiation, resulting in complete remyelination and a thickening of the myelin sheath. These results highlight the importance of targeting microglia during the repair processes in order to enhance remyelination.es_ES
dc.description.sponsorshipThis work was supported by grants from the Ministerio de Economía y Competitividad (MINECO SAF2013-42784-R, SAF2016 76449-R), and the Red Española de Esclerosis Múltiple (REEM: RD12/0032/0008, RD16/0015/0021) sponsored by the Fondo de Investigación Sanitaria (FIS).es_ES
dc.language.isoenges_ES
dc.publisherElsevieres_ES
dc.relationMINECO/ICTI2013-2016/SAF2013-42784-Res_ES
dc.relationMINECO/ICTI2013-2016/SAF2016 76449-Res_ES
dc.relation.isversionofPublisher's versiones_ES
dc.rightsopenAccesses_ES
dc.subjectRemyelinationes_ES
dc.subjectEndocannabinoidses_ES
dc.subjectMicrogliaes_ES
dc.subjectPhagocytosises_ES
dc.subjectTMEVes_ES
dc.titleThe endocannabinoid 2-AG enhances spontaneous remyelination by targeting microgliaes_ES
dc.typeartículoes_ES
dc.identifier.doi10.1016/j.bbi.2018.12.013-
dc.description.peerreviewedPeer reviewedes_ES
dc.relation.publisherversionhttps://doi.org/10.1016/j.bbi.2018.12.013es_ES
dc.identifier.e-issn1090-2139-
dc.rights.licensehttps://creativecommons.org/licenses/by-nc-nd/4.0/es_ES
dc.contributor.funderMinisterio de Economía y Competitividad (España)es_ES
dc.contributor.funderRed Española de Esclerosis Múltiplees_ES
dc.contributor.funderInstituto de Salud Carlos IIIes_ES
dc.relation.csices_ES
oprm.item.hasRevisionno ko 0 false*
dc.identifier.funderhttp://dx.doi.org/10.13039/501100003329es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100004587es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100007747es_ES
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