Evidence map›Paper›PMID 24290728›Full record

ArticleBiological psychiatry2014

WWC1 genotype modulates age-related decline in episodic memory function across the adult life span.

John Muse, Matthew Emery, Fabio Sambataro, Herve Lemaitre, Hao-Yang Tan, Qiang Chen, Bhaskar S Kolachana, Saumitra Das, Joseph H Callicott, Daniel R Weinberger and 1 more

Abstract read
In one paragraph

Article in Biological psychiatry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Genes · 2023
    Pooled it
  2. Long-read whole-genome sequencing of SHR rat substrains with distinct substance use phenotypes.Mammalian genome : official journal of the International Mammalian Genome Society · 2025
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  6. Article
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  8. KIBRA T allele influences memory performance and progression of cognitive decline: a 7-year follow-up study in subjective cognitive decline and mild cognitive impairment.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2019
    Article
  9. Article
  10. Article
  11. Article
  12. Age-Modulated Associations betweenFrontiers in aging neuroscience · 2017
    Article
  13. Impact of KIBRA Polymorphism on Memory Function and the Hippocampus in Older Adults.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2016
    Article
  14. Serum KIBRA mRNA and Protein Expression and Cognitive Functions in Depression.Medical science monitor : international medical journal of experimental and clinical research · 2016
    Article
  15. Review
  16. APOE ε4 genotype predicts memory for everyday activities.Neuropsychology, development, and cognition. Section B, Aging, neuropsychology and cognition · 2015
    Article
  17. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 1 country.

John MuseClinical Brain Disorders Branch (JM, ME, FS, HL, H-YT, QC, BSK, SD, JHC, DRW, VSM), Genes Cognition and Psychosis Program, Intramural Research Program, National Institute of Mental Health, National Institutes of Health, Bethesda; Lieber Institute for Brain Development (JM, H-YT, QC, DRW, VSM), Johns Hopkins University Medical Campus, Baltimore.
Matthew EmeryClinical Brain Disorders Branch (JM, ME, FS, HL, H-YT, QC, BSK, SD, JHC, DRW, VSM), Genes Cognition and Psychosis Program, Intramural Research Program, National Institute of Mental Health, National Institutes of Health, Bethesda.
Fabio SambataroClinical Brain Disorders Branch (JM, ME, FS, HL, H-YT, QC, BSK, SD, JHC, DRW, VSM), Genes Cognition and Psychosis Program, Intramural Research Program, National Institute of Mental Health, National Institutes of Health, Bethesda.
Herve LemaitreClinical Brain Disorders Branch (JM, ME, FS, HL, H-YT, QC, BSK, SD, JHC, DRW, VSM), Genes Cognition and Psychosis Program, Intramural Research Program, National Institute of Mental Health, National Institutes of Health, Bethesda.
Hao-Yang TanClinical Brain Disorders Branch (JM, ME, FS, HL, H-YT, QC, BSK, SD, JHC, DRW, VSM), Genes Cognition and Psychosis Program, Intramural Research Program, National Institute of Mental Health, National Institutes of Health, Bethesda; Lieber Institute for Brain Development (JM, H-YT, QC, DRW, VSM), Johns Hopkins University Medical Campus, Baltimore.
Qiang ChenClinical Brain Disorders Branch (JM, ME, FS, HL, H-YT, QC, BSK, SD, JHC, DRW, VSM), Genes Cognition and Psychosis Program, Intramural Research Program, National Institute of Mental Health, National Institutes of Health, Bethesda; Lieber Institute for Brain Development (JM, H-YT, QC, DRW, VSM), Johns Hopkins University Medical Campus, Baltimore.
Bhaskar S KolachanaClinical Brain Disorders Branch (JM, ME, FS, HL, H-YT, QC, BSK, SD, JHC, DRW, VSM), Genes Cognition and Psychosis Program, Intramural Research Program, National Institute of Mental Health, National Institutes of Health, Bethesda.
Saumitra DasClinical Brain Disorders Branch (JM, ME, FS, HL, H-YT, QC, BSK, SD, JHC, DRW, VSM), Genes Cognition and Psychosis Program, Intramural Research Program, National Institute of Mental Health, National Institutes of Health, Bethesda.
Joseph H CallicottClinical Brain Disorders Branch (JM, ME, FS, HL, H-YT, QC, BSK, SD, JHC, DRW, VSM), Genes Cognition and Psychosis Program, Intramural Research Program, National Institute of Mental Health, National Institutes of Health, Bethesda.
Daniel R WeinbergerClinical Brain Disorders Branch (JM, ME, FS, HL, H-YT, QC, BSK, SD, JHC, DRW, VSM), Genes Cognition and Psychosis Program, Intramural Research Program, National Institute of Mental Health, National Institutes of Health, Bethesda; Lieber Institute for Brain Development (JM, H-YT, QC, DRW, VSM), Johns Hopkins University Medical Campus, Baltimore; Departments of Neurology (DRW); Psychiatry, Neuroscience and the Institute of Genetic Medicine (DRW), Johns Hopkins University School of Medicine, Baltimore, Maryland.
Venkata S MattayClinical Brain Disorders Branch (JM, ME, FS, HL, H-YT, QC, BSK, SD, JHC, DRW, VSM), Genes Cognition and Psychosis Program, Intramural Research Program, National Institute of Mental Health, National Institutes of Health, Bethesda; Lieber Institute for Brain Development (JM, H-YT, QC, DRW, VSM), Johns Hopkins University Medical Campus, Baltimore. Electronic address: anand.mattay@libd.org.
National Institute of Mental Health · USNational Institutes of Health · USJohns Hopkins University · USLieber Institute for Brain Development · US

Funding

Multimodal Imaging: Genetic and Environmental Effects in NeuropsychiatryZIAMH002942 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI BERMAN, KAREN FAITH · 2013 to 2022
$12.2M
Neuroimaging Core FacilityZ01MH002905 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI WEINBERGER, DANIEL · 2007 to 2008
$2.6M
Intramural NIH HHS Z01 MH002905Intramural NIH HHS Z99 MH999999
6 · The paper itself

Abstract

backgroundEpisodic memory (EM) declines with age and the rate of decline is variable across individuals. A single nucleotide polymorphism (rs17070145) in the WWC1 gene that encodes the KIBRA protein critical for long-term potentiation and memory consolidation has previously been associated with EM performance, as well as differences in hippocampal engagement during EM tasks using functional magnetic resonance imaging (fMRI). In the current study, we explore the effect of this polymorphism on EM-related activity and cognitive performance across the adult life span using fMRI.

methodsTwo hundred thirty-two healthy, Caucasian subjects (18-89 years) completed a battery of cognitive tests, as well as an EM task during an fMRI scan.

resultsWWC1 T carriers had significantly better delayed recall performance than CC individuals (p = .006). The relationship between increasing age and recall scores (immediate and delayed) was also significantly different between WWC1 genotype groups (p = .01). In addition to the age-related decline in hippocampal formation (HF) activation (p < .05; false discovery ratesmall volume correction-HF-region of interest), we observed an age by WWC1 genotype interaction on HF activation during encoding and retrieval. The CC group showed a significant negative association between HF activity and increasing age, while no such association was observed in the T carrier group (left HF p = .04; r-z correlation difference during encoding and retrieval; right HF p = .0008; r-z correlation difference during retrieval).

conclusionsOur results show a dynamic relationship between rs17070145 polymorphism and increasing age on neuronal activity in the hippocampal region.

Indexed as

Memory, EpisodicPolymorphism, Single NucleotideAdolescentAdultAgedAged, 80 and overAgingBrainBrain MappingGenotypeHippocampusHumansIntracellular Signaling Peptides and ProteinsLearningMagnetic Resonance ImagingMental RecallIntracellular Signaling Peptides and ProteinsPhosphoproteinsWWC1 protein, humanAgingepisodic memory (EM)hippocampusKIBRAlong-term potentiation (LTP)single nucleotide polymorphism (SNP)WWC1

Identifiers

PMID24290728
PMCPMC3989426
OpenAlexW1993621551

What OpenQuestion holds

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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.