Evidence map›Paper›PMID 27460150›Full record

ArticleNeurobiology of aging2016

Systems genetics identifies Hp1bp3 as a novel modulator of cognitive aging.

Sarah M Neuner, Benjamin P Garfinkel, Lynda A Wilmott, Bogna M Ignatowska-Jankowska, Ami Citri, Joseph Orly, Lu Lu, Rupert W Overall, Megan K Mulligan, Gerd Kempermann and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Neurobiology of aging, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 4 institutions in 3 countries.

Sarah M NeunerDepartment of Anatomy and Neurobiology, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
Benjamin P GarfinkelDepartment of Biological Chemistry, The Alexander Silberman Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem 91904, Israel; The Edmond and Lily Safra Center for Brain Sciences, The Hebrew University of Jerusalem, Jerusalem 91904, Israel.
Lynda A WilmottDepartment of Anatomy and Neurobiology, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
Bogna M Ignatowska-JankowskaThe Edmond and Lily Safra Center for Brain Sciences, The Hebrew University of Jerusalem, Jerusalem 91904, Israel.
Ami CitriThe Edmond and Lily Safra Center for Brain Sciences, The Hebrew University of Jerusalem, Jerusalem 91904, Israel.
Joseph OrlyDepartment of Biological Chemistry, The Alexander Silberman Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem 91904, Israel.
Lu LuDepartment of Genetics, Genomics, and Informatics, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
Rupert W OverallCRTD-Center for Regenerative Therapies Dresden, Technische Universität Dresden, Dresden 01307, Germany.
Megan K MulliganDepartment of Genetics, Genomics, and Informatics, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
Gerd KempermannCRTD-Center for Regenerative Therapies Dresden, Technische Universität Dresden, Dresden 01307, Germany; German Center for Neurodegenerative Diseases (DZNE) Dresden, Dresden 01307, Germany.
Robert W WilliamsDepartment of Genetics, Genomics, and Informatics, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
Kristen M S O'ConnellDepartment of Physiology, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
Catherine C KaczorowskiDepartment of Anatomy and Neurobiology, University of Tennessee Health Science Center, Memphis, TN 38163, USA. Electronic address: ckaczoro@uthsc.edu.
University of Tennessee Health Science Center · USHebrew University of Jerusalem · ILGerman Center for Neurodegenerative Diseases · DETechnische Universität Dresden · DE

Funding

University of Kentucky Alzheimer's Disease Core Center - Biomarker CoreP30AG028383 · NIA · UNIVERSITY OF KENTUCKY · PI VAN ELDIK, LINDA J · 2006 to 2020
$23.3M
Systems Genetics of Alcohol Response and Stress Effects in CNSU01AA013499 · NIAAA · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI WILLIAMS, ROBERT W. · 2002 to 2016
$4.8M
INIA-STRESS: Informatics and Analysis CoreU01AA016662 · NIAAA · VIRGINIA COMMONWEALTH UNIVERSITY · PI WILLIAMS, ROBERT W. · 2007 to 2016
$2.9M
Translational Systems Genetics of Mitochondria, Metabolism, and AgingR01AG043930 · NIA · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI WILLIAMS, ROBERT W. · 2013 to 2017
$2.5M
Modulation of AgRP Neuronal Excitability: Role of Diet and Body WeightR01DK102918 · NIDDK · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI O'CONNELL, KRISTEN M · 2014 to 2018
$2.0M
Proteomics of memory failure: unraveling the relationship between 'normal' brainR00AG039511 · NIA · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI KACZOROWSKI, CATHERINE COOK · 2013 to 2015
$730k
Identification of Genetic Modifiers of Neuronal Deficits and Memory Failure in Alzheimers DiseaseF31AG050357 · NIA · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI NEUNER, SARAH M · 2015 to 2018
$171k
NIAAA NIH HHS U01 AA013499NIAAA NIH HHS U01 AA016662NIA NIH HHS F31 AG050357NIA NIH HHS P30 AG028383NIA NIH HHS R00 AG039511NIA NIH HHS R01 AG043930NIDDK NIH HHS R01 DK102918
6 · The paper itself

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.

Indexed as

Genetic Association StudiesAgingAnimalsCognitionCognition DisordersCognitive AgingConditioning, PsychologicalDisease Models, AnimalFearFemaleGenetic Predisposition to DiseaseHumansMaleMemoryMemory DisordersMiceHP1BP3 protein, mouseNuclear ProteinsBXDCognitive agingFear conditioningGene set enrichment analysisSystems genetics

Identifiers

PMID27460150
PMCPMC5018442
OpenAlexW2431991129

What OpenQuestion holds

Textmetadata
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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.