Home > Publications Database > Systems genetics identifies Hp1bp3 as a novel modulator of cognitive aging. > print

001     138861
005     20240321220519.0
024 7 _ |a 10.1016/j.neurobiolaging.2016.06.008
|2 doi
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024 7 _ |a pmc:PMC5018442
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024 7 _ |a 0197-4580
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024 7 _ |a 1558-1497
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024 7 _ |a altmetric:8848994
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037 _ _ |a DZNE-2020-05183
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Neuner, Sarah M
|b 0
245 _ _ |a Systems genetics identifies Hp1bp3 as a novel modulator of cognitive aging.
260 _ _ |a Amsterdam [u.a.]
|c 2016
|b Elsevier Science
264 _ 1 |3 print
|2 Crossref
|b Elsevier BV
|c 2016-10-01
336 7 _ |a article
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336 7 _ |a ARTICLE
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336 7 _ |a JOURNAL_ARTICLE
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336 7 _ |a Journal Article
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520 _ _ |a 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.
536 _ _ |a 342 - Disease Mechanisms and Model Systems (POF3-342)
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542 _ _ |i 2016-10-01
|2 Crossref
|u https://www.elsevier.com/tdm/userlicense/1.0/
542 _ _ |i 2016-06-18
|2 Crossref
|u http://creativecommons.org/licenses/by-nc-nd/4.0/
588 _ _ |a Dataset connected to CrossRef, PubMed,
650 _ 7 |a HP1BP3 protein, mouse
|2 NLM Chemicals
650 _ 7 |a Nuclear Proteins
|2 NLM Chemicals
650 _ 2 |a Aging: genetics
|2 MeSH
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Cognition: physiology
|2 MeSH
650 _ 2 |a Cognition Disorders: genetics
|2 MeSH
650 _ 2 |a Cognition Disorders: psychology
|2 MeSH
650 _ 2 |a Cognitive Aging: physiology
|2 MeSH
650 _ 2 |a Conditioning, Psychological: physiology
|2 MeSH
650 _ 2 |a Disease Models, Animal
|2 MeSH
650 _ 2 |a Fear
|2 MeSH
650 _ 2 |a Female
|2 MeSH
650 _ 2 |a Genetic Association Studies
|2 MeSH
650 _ 2 |a Genetic Predisposition to Disease: genetics
|2 MeSH
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Male
|2 MeSH
650 _ 2 |a Memory: physiology
|2 MeSH
650 _ 2 |a Memory Disorders: genetics
|2 MeSH
650 _ 2 |a Memory Disorders: psychology
|2 MeSH
650 _ 2 |a Mice
|2 MeSH
650 _ 2 |a Mice, Knockout
|2 MeSH
650 _ 2 |a Nuclear Proteins: physiology
|2 MeSH
700 1 _ |a Garfinkel, Benjamin P
|b 1
700 1 _ |a Wilmott, Lynda A
|b 2
700 1 _ |a Ignatowska-Jankowska, Bogna M
|b 3
700 1 _ |a Citri, Ami
|b 4
700 1 _ |a Orly, Joseph
|b 5
700 1 _ |a Lu, Lu
|b 6
700 1 _ |a Overall, Rupert W
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700 1 _ |a Kempermann, Gerd
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700 1 _ |a Mulligan, Megan K
|b 9
700 1 _ |a Williams, Robert W
|b 10
700 1 _ |a O'Connell, Kristen M S
|b 11
700 1 _ |a Kaczorowski, Catherine C
|b 12
773 1 8 |a 10.1016/j.neurobiolaging.2016.06.008
|b : Elsevier BV, 2016-10-01
|p 58-67
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|t Neurobiology of Aging
|v 46
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773 _ _ |a 10.1016/j.neurobiolaging.2016.06.008
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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