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dc.creatorDurand, Daniela Elizabeth-
dc.creatorCarniglia, Lila-
dc.creatorTurati, Juan-
dc.creatorRamírez, Delia-
dc.creatorSaba, Julieta-
dc.creatorCaruso, Carla Mariana-
dc.creatorLasaga, Mercedes Isabel-
dc.date2019-01-09T20:04:29Z-
dc.date2019-01-09T20:04:29Z-
dc.date2017-09-
dc.date2018-06-06T13:45:00Z-
dc.date.accessioned2019-04-29T15:50:19Z-
dc.date.available2019-04-29T15:50:19Z-
dc.date.issued2017-09-
dc.identifierDurand, Daniela Elizabeth; Carniglia, Lila; Turati, Juan; Ramírez, Delia; Saba, Julieta; et al.; Amyloid-beta neurotoxicity and clearance are both regulated by glial group II metabotropic glutamate receptors; Pergamon-Elsevier Science Ltd; Neuropharmacology; 123; 9-2017; 274-286-
dc.identifier0028-3908-
dc.identifierhttp://hdl.handle.net/11336/67832-
dc.identifierCONICET Digital-
dc.identifierCONICET-
dc.identifier.urihttp://rodna.bn.gov.ar:8080/jspui/handle/bnmm/303371-
dc.descriptionAstrocytes are now fully endorsed as key players in CNS functionality and plasticity. We recently showed that metabotropic glutamate receptor 3 (mGlu3R) activation by LY379268 promotes non-amyloidogenic cleavage of amyloid precursor protein (APP) in cultured astrocytes, leading to increased release of neuroprotective sAPPα. Furthermore, mGlu3R expression is reduced in hippocampal astrocytes from PDAPP-J20 mice, suggesting a role for these receptors in Alzheimer's disease. The present study enquires into the role of astroglial-derived neurotrophins induced by mGlu3R activation in neurotoxicity triggered by amyloid β (Aβ). Conditioned medium from LY379268-treated astrocytes protected hippocampal neurons from Aβ-induced cell death. Immunodepletion of sAPPα from the conditioned medium prevented its protective effect. LY379268 induced brain-derived neurotrophic factor (BDNF) expression in astrocytes, and neutralizing BDNF from conditioned medium also prevented its neuroprotective effect on Aβ neurotoxicity. LY379268 was also able to decrease Aβ-induced neuron death by acting directly on neuronal mGlu3R. On the other hand, LY379268 increased Aβ uptake in astrocytes and microglia. Indeed, and more importantly, a reduction in Aβ-induced neuron death was observed when co-cultured with LY379268-pretreated astrocytes, suggesting a link between neuroprotection and increased glial phagocytic activity. Altogether, these results indicate a double function for glial mGlu3R activation against Aβ neurotoxicity: (i) it increases the release of protective neurotrophins such as sAPPα and BDNF, and (ii) it induces amyloid removal from extracellular space by glia-mediated phagocytosis.-
dc.descriptionFil: Durand, Daniela Elizabeth. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina-
dc.descriptionFil: Carniglia, Lila. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina-
dc.descriptionFil: Turati, Juan. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina-
dc.descriptionFil: Ramírez, Delia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina-
dc.descriptionFil: Saba, Julieta. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina-
dc.descriptionFil: Caruso, Carla Mariana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina-
dc.descriptionFil: Lasaga, Mercedes Isabel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina-
dc.formatapplication/pdf-
dc.formatapplication/pdf-
dc.formatapplication/pdf-
dc.formatapplication/pdf-
dc.formatapplication/pdf-
dc.languageeng-
dc.publisherPergamon-Elsevier Science Ltd-
dc.relationinfo:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1016/j.neuropharm.2017.05.008-
dc.relationinfo:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0028390817302046-
dc.rightsinfo:eu-repo/semantics/restrictedAccess-
dc.rightshttps://creativecommons.org/licenses/by-nc-nd/2.5/ar/-
dc.sourcereponame:CONICET Digital (CONICET)-
dc.sourceinstname:Consejo Nacional de Investigaciones Científicas y Técnicas-
dc.sourceinstacron:CONICET-
dc.subjectALZHEIMER'S DISEASE-
dc.subjectAMYLOID Β CLEARANCE-
dc.subjectBDNF-
dc.subjectMETABOTROPIC GLUTAMATE RECEPTORS-
dc.subjectNEURON-GLIA INTERACTION-
dc.subjectSAPPΑ-
dc.subjectInmunología-
dc.subjectMedicina Básica-
dc.subjectCIENCIAS MÉDICAS Y DE LA SALUD-
dc.titleAmyloid-beta neurotoxicity and clearance are both regulated by glial group II metabotropic glutamate receptors-
dc.typeinfo:eu-repo/semantics/article-
dc.typeinfo:eu-repo/semantics/publishedVersion-
dc.typeinfo:ar-repo/semantics/articulo-
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