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@ARTICLE{Neuner:138861,
      author       = {Neuner, Sarah M and Garfinkel, Benjamin P and Wilmott,
                      Lynda A and Ignatowska-Jankowska, Bogna M and Citri, Ami and
                      Orly, Joseph and Lu, Lu and Overall, Rupert W and
                      Kempermann, Gerd and Mulligan, Megan K and Williams, Robert
                      W and O'Connell, Kristen M S and Kaczorowski, Catherine C},
      title        = {{S}ystems genetics identifies {H}p1bp3 as a novel modulator
                      of cognitive aging.},
      journal      = {Neurobiology of aging},
      volume       = {46},
      issn         = {0197-4580},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier Science},
      reportid     = {DZNE-2020-05183},
      pages        = {58-67},
      year         = {2016},
      abstract     = {An 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.},
      keywords     = {Aging: genetics / Animals / Cognition: physiology /
                      Cognition Disorders: genetics / Cognition Disorders:
                      psychology / Cognitive Aging: physiology / Conditioning,
                      Psychological: physiology / Disease Models, Animal / Fear /
                      Female / Genetic Association Studies / Genetic
                      Predisposition to Disease: genetics / Humans / Male /
                      Memory: physiology / Memory Disorders: genetics / Memory
                      Disorders: psychology / Mice / Mice, Knockout / Nuclear
                      Proteins: physiology / HP1BP3 protein, mouse (NLM Chemicals)
                      / Nuclear Proteins (NLM Chemicals)},
      cin          = {AG Kempermann},
      ddc          = {610},
      cid          = {I:(DE-2719)1710001},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:27460150},
      pmc          = {pmc:PMC5018442},
      doi          = {10.1016/j.neurobiolaging.2016.06.008},
      url          = {https://pub.dzne.de/record/138861},
}