Evidence map›Paper›PMID 24567911›Full record

ArticleNeuroImage. Clinical2014

Disrupted working memory circuitry and psychotic symptoms in 22q11.2 deletion syndrome.

C A Montojo, A Ibrahim, K H Karlsgodt, C Chow, A E Hilton, R K Jonas, T K Vesagas, C E Bearden

Open access · goldAbstract read
In one paragraph

Article in NeuroImage. Clinical, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

13 citing papers in PubMed, 28 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

8 authors at 2 institutions in 1 country.

C A MontojoSemel Institute for Neuroscience and Human Behavior, 760 Westwood Plaza, University of California, Los Angeles, Los Angeles, CA 90095, USA ; Department of Psychology, 1285 Franz Hall, University of California, Los Angeles, Los Angeles, CA 90095, USA.
A IbrahimSemel Institute for Neuroscience and Human Behavior, 760 Westwood Plaza, University of California, Los Angeles, Los Angeles, CA 90095, USA.
K H KarlsgodtFeinstein Institute for Medical Research, Zucker Hillside Hospital, North Shore-LIJ Health System, 350 Community Drive, Manhasset, NY 11030, USA.
C ChowSemel Institute for Neuroscience and Human Behavior, 760 Westwood Plaza, University of California, Los Angeles, Los Angeles, CA 90095, USA.
A E HiltonDepartment of Psychology, 1285 Franz Hall, University of California, Los Angeles, Los Angeles, CA 90095, USA.
R K JonasSemel Institute for Neuroscience and Human Behavior, 760 Westwood Plaza, University of California, Los Angeles, Los Angeles, CA 90095, USA.
T K VesagasSemel Institute for Neuroscience and Human Behavior, 760 Westwood Plaza, University of California, Los Angeles, Los Angeles, CA 90095, USA.
C E BeardenSemel Institute for Neuroscience and Human Behavior, 760 Westwood Plaza, University of California, Los Angeles, Los Angeles, CA 90095, USA ; Department of Psychology, 1285 Franz Hall, University of California, Los Angeles, Los Angeles, CA 90095, USA ; Brain Research Institute, 695 Charles E Young Drive S, University of California, Los Angeles, Los Angeles, CA 90095, USA.
University of California, Los Angeles · USNorthwell Health · US

Funding

Understanding Repetitive Behavior in AutismP50HD055784 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BOOKHEIMER, SUSAN Y · 2007 to 2021
$32.0M
Neurodevelopment and Psychosis in the 22q11.2 Deletion SyndromeR01MH085953 · NIMH · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BEARDEN, CARRIE E · 2010 to 2020
$6.2M
Human Translational Applications Core (HTA - Core) (7 of 8)PL1MH083271 · NIMH · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BILDER, ROBERT M · 2007 to 2011
$5.8M
Neurodevelopment and Psychosis in the 22q11.2 Copy Number VariantsR37MH085953 · NIMH · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CARRIE E BEARDEN · 2023 to 2026
$2.9M
Consortium for Neuropsychiatric Phenomics-Coordinating Center (1 of 8)UL1DE019580 · NIDCR · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BILDER, ROBERT M · 2008 to 2011
$1.9M
Response Inhibition and Dopamine Neurotransmission (RI) (4 of 8)RL1DA024853 · NIDA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LONDON, EDYTHE DANICK · 2007 to 2011
$1.7M
Training in Early Detection and Prevention in Psychiatric DisordersT32MH082719 · NIMH · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CRASKE, MICHELLE G · 2009 to 2013
$999k
NICHD NIH HHS P50 HD055784NICHD NIH HHS P50-HD-055784NIDA NIH HHS RL1 DA024853NIDCR NIH HHS UL1 DE019580NIDCR NIH HHS UL1-DE019580NIMH NIH HHS 5T32MH082719-04NIMH NIH HHS PL1 MH083271NIMH NIH HHS PL1MH083271NIMH NIH HHS R01 MH085953NIMH NIH HHS R01MH085953NIMH NIH HHS R37 MH085953NIMH NIH HHS T32 MH082719
6 · The paper itself

Abstract

22q11.2 deletion syndrome (22q11DS) is a recurrent genetic mutation that is highly penetrant for psychosis. Behavioral research suggests that 22q11DS patients exhibit a characteristic neurocognitive phenotype that includes differential impairment in spatial working memory (WM). Notably, spatial WM has also been proposed as an endophenotype for idiopathic psychotic disorder, yet little is known about the neurobiological substrates of WM in 22q11DS. In order to investigate the neural systems engaged during spatial WM in 22q11DS patients, we collected functional magnetic resonance imaging (fMRI) data while 41 participants (16 22q11DS patients, 25 demographically matched controls) performed a spatial capacity WM task that included manipulations of delay length and load level. Relative to controls, 22q11DS patients showed reduced neural activation during task performance in the intraparietal sulcus (IPS) and superior frontal sulcus (SFS). In addition, the typical increases in neural activity within spatial WM-relevant regions with greater memory load were not observed in 22q11DS. We further investigated whether neural dysfunction during WM was associated with behavioral WM performance, assessed via the University of Maryland letter-number sequencing (LNS) task, and positive psychotic symptoms, assessed via the Structured Interview for Prodromal Syndromes (SIPS), in 22q11DS patients. WM load activity within IPS and SFS was positively correlated with LNS task performance; moreover, WM load activity within IPS was inversely correlated with the severity of unusual thought content and delusional ideas, indicating that decreased recruitment of working memory-associated neural circuitry is associated with more severe positive symptoms. These results suggest that 22q11DS patients show reduced neural recruitment of brain regions critical for spatial WM function, which may be related to characteristic behavioral manifestations of the disorder.

Indexed as

Memory, Short-TermAdolescentAdultBrainConnectomeDiGeorge SyndromeFemaleHumansMagnetic Resonance ImagingMaleMemory DisordersNerve NetNeural PathwaysPsychotic DisordersReproducibility of ResultsSensitivity and SpecificityCopy number variationEndophenotypeExecutive functionPsychosisVelocardiofacial syndrome

Identifiers

PMID24567911
PMCPMC3930118
OpenAlexW2003122167

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.