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dc.contributor.authorColié, Sandra
dc.contributor.authorSarroca, Sara
dc.contributor.authorPalenzuela Muñoz, Rocío 
dc.contributor.authorGarcía, Idoia
dc.contributor.authorMatheu, Ander
dc.contributor.authorCorpas, Rubén
dc.contributor.authorDotti, Carlos G.
dc.contributor.authorEsteban, José A.
dc.contributor.authorSanfeliu, Coral
dc.contributor.authorNebreda, Ángel R.
dc.date.accessioned2017-09-18T11:36:39Z
dc.date.available2017-09-18T11:36:39Z
dc.date.issued2017-03-31
dc.identifier.issn2045-2322
dc.identifier.urihttp://hdl.handle.net/10641/1334
dc.description.abstractAlzheimer’s disease (AD) is a neurodegenerative disorder characterized by a severe and progressive neuronal loss leading to cognitive dysfunctions. Previous reports, based on the use of chemical inhibitors, have connected the stress kinase p38α to neuroinflammation, neuronal death and synaptic dysfunction. To explore the specific role of neuronal p38α signalling in the appearance of pathological symptoms, we have generated mice that combine expression of the 5XFAD transgenes to induce AD symptoms with the downregulation of p38α only in neurons (5XFAD/p38α∆-N). We found that the neuronal-specific deletion of p38α improves the memory loss and long-term potentiation impairment induced by 5XFAD transgenes. Furthermore, 5XFAD/p38α∆-N mice display reduced amyloid-β accumulation, improved neurogenesis, and important changes in brain cytokine expression compared with 5XFAD mice. Our results implicate neuronal p38α signalling in the synaptic plasticity dysfunction and memory impairment observed in 5XFAD mice, by regulating both amyloid-β deposition in the brain and the relay of this accumulation to mount an inflammatory response, which leads to the cognitive deficits.eng
dc.language.isoengspa
dc.publisherScientific Reportsspa
dc.rightsAtribución-NoComercial-SinDerivadas 3.0 España*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/es/*
dc.subjectAlzheimerspa
dc.titleNeuronal p38α mediates synaptic and cognitive dysfunction in an Alzheimer’s mouse model by controlling β-amyloid production.spa
dc.typearticlespa
dc.description.versionpost-printspa
dc.rights.accessRightsopenAccessspa
dc.description.extent1848 KBspa


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