Evidence map›Paper›PMID 21878355›Full record

ReviewBehavioural brain research2011

Genetic influence on the working memory circuitry: behavior, structure, function and extensions to illness.

Katherine H Karlsgodt, Peter Bachman, Anderson M Winkler, Carrie E Bearden, David C Glahn

Open access · greenAbstract readReview
In one paragraph

Review in Behavioural brain research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

20 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Association ofFrontiers in neuroscience · 2022
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Clinical significance of knowledge about the structure, function, and impairments of working memory.Medical science monitor : international medical journal of experimental and clinical research · 2013
    Review
  20. Article
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

5 authors at 4 institutions in 1 country.

Katherine H KarlsgodtDepartment of Psychiatry and Biobehavioral Sciences, Semel Institute for Neuroscience and Human Behavior, University of California Los Angeles, Los Angeles, CA, USA. kkarlsgo@ucla.edu
Peter Bachman
Anderson M Winkler
Carrie E Bearden
David C Glahn
University of California, Los Angeles · USHartford Hospital · USNeurobehavioral Systems · USYale University · US

Funding

Neurodevelopment and Psychosis in the 22q11.2 Deletion SyndromeR01MH085953 · NIMH · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BEARDEN, CARRIE E · 2010 to 2020
$6.2M
Genetics of Brain Structure and FunctionR01MH078143 · NIMH · YALE UNIVERSITY · PI GLAHN, DAVID C · 2006 to 2014
$4.3M
Genetics of Brain Structure and Function: Genome-Wide AssociationR01MH083824 · NIMH · YALE UNIVERSITY · PI GLAHN, DAVID C · 2008 to 2013
$3.3M
Influence of Psychosis on Brain-Behavior Endophenotypes for Bipolar DisorderR01MH080912 · NIMH · YALE UNIVERSITY · PI GLAHN, DAVID C · 2008 to 2012
$2.6M
WNTs, FGFs, and BMPs Induce and Maintain the TelencephalonR01MH083804 · NIMH · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI HEBERT, JEAN M · 2009 to 2013
$2.0M
NIMH NIH HHS R01 MH078143NIMH NIH HHS R01 MH080912NIMH NIH HHS R01 MH083804NIMH NIH HHS R01 MH083824NIMH NIH HHS R01 MH085953NIMH NIH HHS R01MH085953
6 · The paper itself

Abstract

Working memory is a highly heritable complex cognitive trait that is critical for a number of higher-level functions. However, the neural substrates of this behavioral phenotype are intricate and it is unknown through what precise biological mechanism variation in working memory is transmitted. In this review we explore different functional and structural components of the working memory circuitry, and the degree to which each of them is contributed to by genetic factors. Specifically, we consider dopaminergic function, glutamatergic function, white matter integrity and gray matter structure all of which provide potential mechanisms for the inheritance of working memory deficits. In addition to discussing the overall heritability of these measures we also address specific genes that may play a role. Each of these heritable components has the potential to uniquely contribute to the working memory deficits observed in genetic disorders, including 22q deletion syndrome, fragile X syndrome, phenylketonuria (PKU), and schizophrenia. By observing the individual contributions of disruptions in different components of the working memory circuitry to behavioral performance, we highlight the concept that there may be many routes to a working memory deficit; even though the same cognitive measure may be a valid endophenotype across different disorders, the underlying cause of, and treatment for, the deficit may differ. This has implications for our understanding of the transmission of working memory deficits in both healthy and disordered populations.

Indexed as

AnimalsBrainGenetic Diseases, InbornHumansMemory DisordersMemory, Short-TermModels, BiologicalModels, PsychologicalNeural PathwaysNeuroimagingSchizophreniaSynaptic Transmission

Identifiers

PMID21878355
PMCPMC3545474
OpenAlexW2038138414

What OpenQuestion holds

Textmetadata
LicenceTDM
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.