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dc.contributor.authorMitchell, Jacqueline C
dc.contributor.authorAriff, Belall B
dc.contributor.authorYates, Darran M
dc.contributor.authorLau, Kwok-Fai
dc.contributor.authorPerkinton, Michael S
dc.contributor.authorRogelj, Boris
dc.contributor.authorStephenson, John D
dc.contributor.authorMiller, Christopher C J
dc.contributor.authorMcLoughlin, Declan M
dc.date.accessioned2011-04-27T09:19:17Z
dc.date.available2011-04-27T09:19:17Z
dc.date.issued2009-12-01
dc.identifier.citationX11beta rescues memory and long-term potentiation deficits in Alzheimer's disease APPswe Tg2576 mice. 2009, 18 (23):4492-500 Hum. Mol. Genet.en
dc.identifier.issn1460-2083
dc.identifier.pmid19744962
dc.identifier.doi10.1093/hmg/ddp408
dc.identifier.urihttp://hdl.handle.net/10147/128717
dc.description.abstractIncreased production and deposition of amyloid beta-protein (Abeta) are believed to be key pathogenic events in Alzheimer's disease. As such, routes for lowering cerebral Abeta levels represent potential therapeutic targets for Alzheimer's disease. X11beta is a neuronal adaptor protein that binds to the intracellular domain of the amyloid precursor protein (APP). Overexpression of X11beta inhibits Abeta production in a number of experimental systems. However, whether these changes to APP processing and Abeta production induced by X11beta overexpression also induce beneficial effects to memory and synaptic plasticity are not known. We report here that X11beta-mediated reduction in cerebral Abeta is associated with normalization of both cognition and in vivo long-term potentiation in aged APPswe Tg2576 transgenic mice that model the amyloid pathology of Alzheimer's disease. Overexpression of X11beta itself has no detectable adverse effects upon mouse behaviour. These findings support the notion that modulation of X11beta function represents a therapeutic target for Abeta-mediated neuronal dysfunction in Alzheimer's disease.
dc.language.isoenen
dc.subject.meshAlzheimer Disease
dc.subject.meshAmyloid beta-Peptides
dc.subject.meshAmyloid beta-Protein Precursor
dc.subject.meshAnimals
dc.subject.meshBehavior, Animal
dc.subject.meshCarrier Proteins
dc.subject.meshDisease Models, Animal
dc.subject.meshFemale
dc.subject.meshHumans
dc.subject.meshLong-Term Potentiation
dc.subject.meshMale
dc.subject.meshMemory
dc.subject.meshMice
dc.subject.meshMice, Inbred C57BL
dc.subject.meshMice, Transgenic
dc.subject.meshNerve Tissue Proteins
dc.titleX11beta rescues memory and long-term potentiation deficits in Alzheimer's disease APPswe Tg2576 mice.en
dc.typeArticleen
dc.contributor.departmentMRC Centre for Neurodegeneration Research, King's College London, Institute of Psychiatry, London SE5 8AF, UK.en
dc.identifier.journalHuman molecular geneticsen
dc.description.provinceLeinster
refterms.dateFOA2018-08-22T12:12:55Z
html.description.abstractIncreased production and deposition of amyloid beta-protein (Abeta) are believed to be key pathogenic events in Alzheimer's disease. As such, routes for lowering cerebral Abeta levels represent potential therapeutic targets for Alzheimer's disease. X11beta is a neuronal adaptor protein that binds to the intracellular domain of the amyloid precursor protein (APP). Overexpression of X11beta inhibits Abeta production in a number of experimental systems. However, whether these changes to APP processing and Abeta production induced by X11beta overexpression also induce beneficial effects to memory and synaptic plasticity are not known. We report here that X11beta-mediated reduction in cerebral Abeta is associated with normalization of both cognition and in vivo long-term potentiation in aged APPswe Tg2576 transgenic mice that model the amyloid pathology of Alzheimer's disease. Overexpression of X11beta itself has no detectable adverse effects upon mouse behaviour. These findings support the notion that modulation of X11beta function represents a therapeutic target for Abeta-mediated neuronal dysfunction in Alzheimer's disease.


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