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dc.contributor.authorChristian Giaume
dc.contributor.authorAnnette Koulakoff
dc.contributor.authorPascal Ezan
dc.creatorSáez- Juan Carlos
dc.date.accessioned2017-05-03T17:57:39Z
dc.date.available2017-05-03T17:57:39Z
dc.date.issued2010
dc.identifier.urihttp://hdl.handle.net/10533/198097
dc.description.abstractAlzheimer’s disease (AD) is an age-related, neurodegenerative disease that results in memory loss, behavior and personality changes, as well as a decrease in thinking abilities. Among tissue manifestations is included the generation of amyloid plaques into the extracellular brain parenchyma composed by amyloid β (Aβ) peptide 1. Although Aβ-neurotoxicity involves activation of NMDA receptors, sustained elevations of [Ca2+]i, and oxidative stress (Laferla et al., 2007), the full underlying mechanism associated to AD remains to be elucidated. Cerebral cortex and hippocampus from AD patients exhibit a reactive gliosis characterized by activated microglia and astrocytes closely associated with amyloid plaques (Kalaria et al., 1999). It has been noted that the immunoreactivity of Cx43 is increased around amyloid plaques where reactive gliosis occurs (Nagy et al., 1996). The present partnership has already shown that under chronic pathological threatening conditions (e.g., AD) microglia become overactivated and release TNF-α and IL-β two pro-inflammatory molecules that increase HC opening and reduce gap junctional communication in astrocytes, depriving neurons of glial protective functions and further reducing neuronal viability (Orellana et al., 2009). In addition, the cytokine-induced astroglial hemichannel activity is prevented by cannabinoids (Froger et al., 2009), which have been shown to reduce the Aβ- induced neuroinflammation in vivo (Esposito et al., 2007). Indeed, cannabinoids are good candidates to reduce the inflammatory response and gliosis (Cabral and Griffin-Thomas, 2008; Croxford, 2003) and because astrocytes and MG are one of their targets in the central nervous system (Stella, 2004). Increasing number of studies revealed the anti-inflammatory properties of CBs are exerted both in periphery and in CNS (for reviews see Klein et al.. 2003, Klein. 2005; Pacher et al., 2006; Walter and Stella, 2004;
dc.language.isospa
dc.titleRole of Glial Hemichannels in Neurodegenerative Processes: Application to Alzheimer´S Disease
dc.typeProyecto
dc.contributor.corporatenamePontificia Universidad Católica de Chile
dc.contributor.institutionUniversity of Leeds
dc.contributor.institutionEcole des Mines d´Albi
dc.contributor.institutionUniversidad Rio de Janeiro
dc.identifier.folioC10S01
dc.description.statusAprobada
dc.description.conicytinstrumentcontestECOS
dc.description.conicytprogramPrograma de Cooperación Internacional
dc.relation.contestHandle/10533/198095
dc.identifier.generoM
dc.relation.instrumentHandle/10533/108080
dc.relation.programhandle/10533/108039
dc.description.shortconicytprogramPrograma de Cooperación Internacional
dc.date.annoconcurso2010
dc.description.corporaterolIP
dc.subject.fondecyt1nCiencias de la Salud


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