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000138861 0247_ $$2doi$$a10.1016/j.neurobiolaging.2016.06.008
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000138861 0247_ $$2ISSN$$a1558-1497
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000138861 037__ $$aDZNE-2020-05183
000138861 041__ $$aEnglish
000138861 082__ $$a610
000138861 1001_ $$aNeuner, Sarah M$$b0
000138861 245__ $$aSystems genetics identifies Hp1bp3 as a novel modulator of cognitive aging.
000138861 260__ $$aAmsterdam [u.a.]$$bElsevier Science$$c2016
000138861 264_1 $$2Crossref$$3print$$bElsevier BV$$c2016-10-01
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000138861 520__ $$aAn individual's genetic makeup plays an important role in determining susceptibility to cognitive aging. Identifying the specific genes that contribute to cognitive aging may aid in early diagnosis of at-risk patients, as well as identify novel therapeutics targets to treat or prevent development of symptoms. Challenges to identifying these specific genes in human studies include complex genetics, difficulty in controlling environmental factors, and limited access to human brain tissue. Here, we identify Hp1bp3 as a novel modulator of cognitive aging using a genetically diverse population of mice and confirm that HP1BP3 protein levels are significantly reduced in the hippocampi of cognitively impaired elderly humans relative to cognitively intact controls. Deletion of functional Hp1bp3 in mice recapitulates memory deficits characteristic of aged impaired mice and humans, further supporting the idea that Hp1bp3 and associated molecular networks are modulators of cognitive aging. Overall, our results suggest Hp1bp3 may serve as a potential target against cognitive aging and demonstrate the utility of genetically diverse animal models for the study of complex human disease.
000138861 536__ $$0G:(DE-HGF)POF3-342$$a342 - Disease Mechanisms and Model Systems (POF3-342)$$cPOF3-342$$fPOF III$$x0
000138861 542__ $$2Crossref$$i2016-10-01$$uhttps://www.elsevier.com/tdm/userlicense/1.0/
000138861 542__ $$2Crossref$$i2016-06-18$$uhttp://creativecommons.org/licenses/by-nc-nd/4.0/
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000138861 650_7 $$2NLM Chemicals$$aHP1BP3 protein, mouse
000138861 650_7 $$2NLM Chemicals$$aNuclear Proteins
000138861 650_2 $$2MeSH$$aAging: genetics
000138861 650_2 $$2MeSH$$aAnimals
000138861 650_2 $$2MeSH$$aCognition: physiology
000138861 650_2 $$2MeSH$$aCognition Disorders: genetics
000138861 650_2 $$2MeSH$$aCognition Disorders: psychology
000138861 650_2 $$2MeSH$$aCognitive Aging: physiology
000138861 650_2 $$2MeSH$$aConditioning, Psychological: physiology
000138861 650_2 $$2MeSH$$aDisease Models, Animal
000138861 650_2 $$2MeSH$$aFear
000138861 650_2 $$2MeSH$$aFemale
000138861 650_2 $$2MeSH$$aGenetic Association Studies
000138861 650_2 $$2MeSH$$aGenetic Predisposition to Disease: genetics
000138861 650_2 $$2MeSH$$aHumans
000138861 650_2 $$2MeSH$$aMale
000138861 650_2 $$2MeSH$$aMemory: physiology
000138861 650_2 $$2MeSH$$aMemory Disorders: genetics
000138861 650_2 $$2MeSH$$aMemory Disorders: psychology
000138861 650_2 $$2MeSH$$aMice
000138861 650_2 $$2MeSH$$aMice, Knockout
000138861 650_2 $$2MeSH$$aNuclear Proteins: physiology
000138861 7001_ $$aGarfinkel, Benjamin P$$b1
000138861 7001_ $$aWilmott, Lynda A$$b2
000138861 7001_ $$aIgnatowska-Jankowska, Bogna M$$b3
000138861 7001_ $$aCitri, Ami$$b4
000138861 7001_ $$aOrly, Joseph$$b5
000138861 7001_ $$aLu, Lu$$b6
000138861 7001_ $$0P:(DE-HGF)0$$aOverall, Rupert W$$b7
000138861 7001_ $$0P:(DE-2719)2000011$$aKempermann, Gerd$$b8$$eCorresponding author$$udzne
000138861 7001_ $$aMulligan, Megan K$$b9
000138861 7001_ $$aWilliams, Robert W$$b10
000138861 7001_ $$aO'Connell, Kristen M S$$b11
000138861 7001_ $$aKaczorowski, Catherine C$$b12
000138861 77318 $$2Crossref$$3journal-article$$a10.1016/j.neurobiolaging.2016.06.008$$b : Elsevier BV, 2016-10-01$$p58-67$$tNeurobiology of Aging$$v46$$x0197-4580$$y2016
000138861 773__ $$0PERI:(DE-600)1498414-3$$a10.1016/j.neurobiolaging.2016.06.008$$gVol. 46, p. 58 - 67$$p58-67$$q46<58 - 67$$tNeurobiology of aging$$v46$$x0197-4580$$y2016
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