Evidence map›Paper›PMID 23549417›Full record

ArticleTranslational psychiatry2013

Unique pharmacological actions of atypical neuroleptic quetiapine: possible role in cell cycle/fate control.

M A Kondo, K Tajinda, C Colantuoni, H Hiyama, S Seshadri, B Huang, S Pou, K Furukori, C Hookway, H Jaaro-Peled and 6 more

Open access · goldAbstract readComparative Study
In one paragraph

Article in Translational psychiatry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

15 citing papers in PubMed, 25 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

16 authors at 4 institutions in 2 countries.

M A KondoDepartment of Psychiatry and Behavioral Sciences, Johns Hopkins School of Medicine, Baltimore, MD, USA.
K Tajinda
C Colantuoni
H Hiyama
S Seshadri
B Huang
S Pou
K Furukori
C Hookway
H Jaaro-Peled
S-i Kano
N Matsuoka
K Harada
K Ni
J Pevsner
A Sawa
Johns Hopkins University · USJohns Hopkins Medicine · USAstellas Pharma (Japan) · JPKennedy Krieger Institute · US

Funding

Project 3P50MH094268 · NIMH · JOHNS HOPKINS UNIVERSITY · PI SAWA, AKIRA · 2011 to 2020
$19.9M
NICHD MENTAL RETARDATION RESEARCH CENTER CORE GRANTP30HD024061 · NICHD · KENNEDY KRIEGER CHILDRENS HOSPITAL · PI VALLE, DAVID · 1988 to 2013
$15.8M
Research Center for Molecular Pathogenesis of SchizophreniaP20MH084018 · NIMH · JOHNS HOPKINS UNIVERSITY · PI SAWA, AKIRA · 2008 to 2010
$3.3M
Nuclear pathway of DISC1 in major mental illnesses: biochemistry and cell biologyR01MH069853 · NIMH · JOHNS HOPKINS UNIVERSITY · PI SAWA, AKIRA · 2004 to 2012
$3.2M
Oxidative stress and schizophrenia: combination of cell biology and brain imagingR01MH092443 · NIMH · JOHNS HOPKINS UNIVERSITY · PI SAWA, AKIRA · 2011 to 2015
$1.8M
Defining of Neurodevelopmental Pathways Regulated by Neuregulin- DISC1 InteractioRC1MH088753 · NIMH · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ANTON, EVA S, SAWA, AKIRA · 2009 to 2010
$933k
PICK1 knockout mice: role for D-serine in neonatal forebrainsR21MH085226 · NIMH · JOHNS HOPKINS UNIVERSITY · PI SAWA, AKIRA · 2010 to 2011
$369k
NICHD NIH HHS HD-24061NICHD NIH HHS P30 HD024061NIMH NIH HHS MH-069853NIMH NIH HHS MH-084018NIMH NIH HHS MH-085226NIMH NIH HHS MH-088753NIMH NIH HHS MH-092443NIMH NIH HHS MH-94268NIMH NIH HHS P20 MH084018NIMH NIH HHS P50 MH094268NIMH NIH HHS R01 MH069853NIMH NIH HHS R01 MH092443NIMH NIH HHS R21 MH085226NIMH NIH HHS RC1 MH088753
6 · The paper itself

Abstract

Quetiapine is an atypical neuroleptic with a pharmacological profile distinct from classic neuroleptics that function primarily via blockade of dopamine D2 receptors. In the United States, quetiapine is currently approved for treating patients with schizophrenia, major depression and bipolar I disorder. Despite its widespread use, its cellular effects remain elusive. To address possible mechanisms, we chronically treated mice with quetiapine, haloperidol or vehicle and examined quetiapine-specific gene expression change in the frontal cortex. Through microarray analysis, we observed that several groups of genes were differentially expressed upon exposure to quetiapine compared with haloperidol or vehicle; among them, Cdkn1a, the gene encoding p21, exhibited the greatest fold change relative to haloperidol. The quetiapine-induced downregulation of p21/Cdkn1a was confirmed by real-time polymerase chain reaction and in situ hybridization. Consistent with single gene-level analyses, functional group analyses also indicated that gene sets associated with cell cycle/fate were differentially regulated in the quetiapine-treated group. In cortical cell cultures treated with quetiapine, p21/Cdkn1a was significantly downregulated in oligodendrocyte precursor cells and neurons, but not in astrocytes. We propose that cell cycle-associated intervention by quetiapine in the frontal cortex may underlie a unique efficacy of quetiapine compared with typical neuroleptics.

Indexed as

Analysis of VarianceAnimalsAntipsychotic AgentsAstrocytesCell CycleDibenzothiazepinesDisease Models, AnimalFrontal LobeGene ExpressionHaloperidolIn Situ HybridizationMaleMethamphetamineMiceNeuronsOligodendrogliaAntipsychotic AgentsDibenzothiazepinesHaloperidolMethamphetaminep21-Activated KinasesQuetiapine Fumarate

Identifiers

PMID23549417
PMCPMC3641406
OpenAlexW2028846654

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.