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dc.contributor.authorRubio, Alicia-
dc.contributor.authorSánchez-Mut, José V.-
dc.contributor.authorGarcía, Esther-
dc.contributor.authorVelasquez, Zahady D.-
dc.contributor.authorOliver de la Cruz, Jorge-
dc.contributor.authorEsteller, Manel-
dc.contributor.authorÁvila, Jesús-
dc.date.accessioned2012-11-02T13:12:51Z-
dc.date.available2012-11-02T13:12:51Z-
dc.date.issued2011-
dc.identifier.citationJournal of Neuroscience Research 90 (1): 13-20 (2011)es_ES
dc.identifier.issn1097-4547-
dc.identifier.urihttp://hdl.handle.net/10261/59393-
dc.description.abstractBeta Amyloid, present in senile plaques, has been related largely to neuronal loss in the brain of patients with Alzheimer’s disease. However, how neurons respond to b amyloid insults is still poorly understood. Here we show that b amyloid increases somatostatin and cortistatin gene expression mainly through an increase in histone 3 lysine 4 methylation (H3K4me3), a modification associated with transcriptional activation. Somatostatin and cortistatin partially decreased b amyloid toxicity in primary cortical neurons in culture. Thus we suggest that neurons respond to b amyloid insults by releasing somatostatin and cortistatin, which will act as a protective agent against b amyloid toxicity. Our results suggest a relevant function for both neuropeptides against b amyloid toxicity, providing new insights into Alzheimer’s diseasees_ES
dc.description.sponsorshipb Amyloid, present in senile plaques, has been related largely to neuronal loss in the brain of patients with Alzheimer’s disease. However, how neurons respond to b amyloid insults is still poorly understood. Here we show that b amyloid increases somatostatin and cortistatin gene expression mainly through an increase in histone 3 lysine 4 methylation (H3K4me3), a modification associated with transcriptional activation. Somatostatin and cortistatin partially decreased b amyloid toxicity in primary cortical neurons in culture. Thus we suggest that neurons respond to b amyloid insults by releasing somatostatin and cortistatin, which will act as a protective agent against b amyloid toxicity. Our results suggest a relevant function for both neuropeptides against b amyloid toxicity, providing new insights into Alzheimer’s diseasees_ES
dc.language.isoenges_ES
dc.publisherJohn Wiley & Sonses_ES
dc.rightsclosedAccesses_ES
dc.subjectSomatostatines_ES
dc.subjectAmyloides_ES
dc.subjectNeuronses_ES
dc.subjectGSK3es_ES
dc.subjectAlzheimer’s diseasees_ES
dc.subjectHistone methylationes_ES
dc.titleEpigenetic Control of Somatostatin and Cortistatin Expression by Beta Amyloid Peptidees_ES
dc.typeartículoes_ES
dc.identifier.doi10.1002/jnr.22731-
dc.description.peerreviewedPeer reviewedes_ES
dc.relation.publisherversionhttp://dx.doi.org/10.1002/jnr.22731es_ES
dc.type.coarhttp://purl.org/coar/resource_type/c_6501es_ES
item.openairetypeartículo-
item.cerifentitytypePublications-
item.languageiso639-1en-
item.grantfulltextnone-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextNo Fulltext-
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