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dc.contributor.authorZhao, Liqin
dc.contributor.authorWoody, Sarah K.
dc.contributor.authorChhibber, Anindit
dc.date.accessioned2017-01-12T18:27:39Z
dc.date.available2017-01-12T18:27:39Z
dc.date.issued2016-11-01
dc.identifier.citationZhao, Liqin, Sarah K. Woody, and Anindit Chhibber. "Estrogen Receptor β in Alzheimerâ s Disease: From Mechanisms to Therapeutics." Ageing Research Reviews 24 (2015): 178-90.en_US
dc.identifier.urihttp://hdl.handle.net/1808/22610
dc.description.abstractAlzheimer's disease (AD) disproportionally affects women and men. The female susceptibility for AD has been largely associated with the loss of ovarian sex hormones during menopause. This review examines current understanding of the role of estrogen receptor β (ERβ) in the regulation of neurological health and its implication in the development and intervention of AD. Since its discovery in 1996, research conducted over the last 15-20 years has documented a great deal of evidence indicating that ERβ plays a pivotal role in a broad spectrum of brain activities from development to aging. ERβ genetic polymorphisms have been associated with cognitive impairment and increased risk for AD predominantly in women. The role of ERβ in the intervention of AD has been demonstrated by the alteration of AD pathology in response to treatment with ERβ-selective modulators in transgenic models that display pronounced plaque and tangle histopathological presentations as well as learning and memory deficits. Future studies that explore the potential interactions between ERβ signaling and the genetic isoforms of human apolipoprotein E (APOE) in brain aging and development of AD-risk phenotype are critically needed. The current trend of lost-in-translation in AD drug development that has primarily been based on early-onset familial AD (FAD) models underscores the urgent need for novel models that recapitulate the etiology of late-onset sporadic AD (SAD), the most common form of AD representing more than 95% of the current human AD population. Combining the use of FAD-related models that generally have excellent face validity with SAD-related models that hold more reliable construct validity would together increase the predictive validity of preclinical findings for successful translation into humans.en_US
dc.publisherElsevier Massonen_US
dc.rightsThis is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License 3.0 (CC BY-NC-ND 3.0 US), which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.en_US
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/
dc.subjectAlzheimer's diseaseen_US
dc.subjectSex differencesen_US
dc.subjectEstrogen receptor βen_US
dc.subjectERβ polymorphismen_US
dc.subjectApolipoprotein Een_US
dc.subjectLate-onset AD modelsen_US
dc.titleEstrogen receptor β in Alzheimer's disease: from mechanisms to therapeuticsen_US
dc.typeArticleen_US
kusw.kuauthorZhao, Liqin
kusw.kudepartmentPharmacology & Toxicologyen_US
dc.identifier.doi10.1016/j.arr.2015.08.001en_US
kusw.oaversionScholarly/refereed, author accepted manuscripten_US
kusw.oapolicyThis item meets KU Open Access policy criteria.en_US
dc.rights.accessrightsopenAccess


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This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License 3.0 (CC BY-NC-ND 3.0 US), which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
Except where otherwise noted, this item's license is described as: This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License 3.0 (CC BY-NC-ND 3.0 US), which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.