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dc.contributor.authorBuendía Abaitua, Izaskun-
dc.contributor.authorEgea Maiquez, Javier-
dc.contributor.authorParada, Esther-
dc.contributor.authorNavarro, Elisa-
dc.contributor.authorLeón Martínez, Rafael-
dc.contributor.authorRodríguez-Franco, María Isabel-
dc.contributor.authorLópez, M. G.-
dc.date.accessioned2015-03-05T11:56:52Z-
dc.date.available2015-03-05T11:56:52Z-
dc.date.issued2015-
dc.identifierdoi: 10.1021/cn5002073-
dc.identifierissn: 1948-7193-
dc.identifiere-issn: 1948-7193-
dc.identifier.citationACS Chemical Neuroscience 6: 288-296 (2015)-
dc.identifier.urihttp://hdl.handle.net/10261/111881-
dc.description.abstractWe have investigated the protective effects of ITH91/IQM157, a hybrid of melatonin and N,N-dibenzyl(N-methyl)amine, in an in vitro model of Alzheimer's disease (AD)-like pathology that combines amyloid beta (Aβ) and tau hyperphosphorylation induced by okadaic acid (OA), in the human neuroblastoma cell line SH-SY5Y. Combination of subtoxic concentrations of Aβ and OA caused a significant toxicity of 40% cell death, which mainly was apoptotic; this effect was accompanied by retraction of the cells' prolongations and accumulation of thioflavin-S stained protein aggregates. In this toxicity model, ITH91/IQM157 (1-1000 nM) reduced cell death measured as MTT reduction; at 100 nM, it prevented apoptosis, retraction of prolongations, and Aβ aggregates. The protective actions of ITH91/IQM157 were blocked by mecamylamine, luzindol, chelerythrine, PD98059, LY294002, and SnPP. We show that the combination of melatonin with a fragment endowed with AChE inhibition in a unique chemical structure, ITH91/IQM157, can reduce neuronal cell death induced by Aβ and OA by a signaling pathway that implicates both nicotinic and melatonin receptors, PKC, Akt, ERK1/2, and induction of hemoxygenase-1.-
dc.publisherAmerican Chemical Society-
dc.relationeu-repo/grant/Agreement/EC/FP7/322156-
dc.relation.isversionofPreprint-
dc.rightsopenAccess-
dc.titleThe melatonin- N,N-dibenzyl(N-methyl)amine hybrid ITH91/IQM157 affords neuroprotection in an in vitro Alzheimer's model via hemo-oxygenase-1 induction-
dc.typeartículo-
dc.identifier.doi10.1021/cn5002073-
dc.date.updated2015-03-05T11:56:52Z-
dc.description.versionPeer Reviewed-
dc.language.rfc3066eng-
dc.contributor.funderEuropean Commission-
dc.contributor.funderInstituto de Salud Carlos III-
dc.contributor.funderMinisterio de Economía y Competitividad (España)-
dc.contributor.funderUniversidad Autónoma de Madrid-
dc.contributor.funderInstituto Fundación Teófilo Hernando-
dc.identifier.funderhttp://dx.doi.org/10.13039/501100000780es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100004587es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100003329es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100004593es_ES
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