X11 beta rescues memory and long-term potentiation deficits in Alzheimer's disease APPswe Tg2576 mice
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AbstractIncreased production and deposition of amyloid beta-protein (A beta) are believed to be key pathogenic events in Alzheimer's disease. As such, routes for lowering cerebral A beta levels represent potential therapeutic targets for Alzheimer's disease. X11 beta is a neuronal adaptor protein that binds to the intracellular domain of the amyloid precursor protein (APP). Overexpression of X11 beta inhibits A beta production in a number of experimental systems. However, whether these changes to APP processing and A beta production induced by X11 beta overexpression also induce beneficial effects to memory and synaptic plasticity are not known. We report here that X11 beta-mediated reduction in cerebral A beta 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 X11 beta itself has no detectable adverse effects upon mouse behaviour. These findings support the notion that modulation of X11 beta function represents a therapeutic target for A beta-mediated neuronal dysfunction in Alzheimer's disease.
All Author(s) ListMitchell JC, Ariff BB, Yates DM, Lau KF, Perkinton MS, Rogelj B, Stephenson JD, Miller CCJ, McLoughlin DM
Journal nameHuman Molecular Genetics
Volume Number18
Issue Number23
PublisherOxford University Press (OUP): Policy B - Oxford Open Option B
Pages4492 - 4500
LanguagesEnglish-United Kingdom
Web of Science Subject CategoriesBiochemistry & Molecular Biology; BIOCHEMISTRY & MOLECULAR BIOLOGY; Genetics & Heredity; GENETICS & HEREDITY

Last updated on 2020-11-01 at 00:37