Evidence map›Paper›PMID 23295814›Full record

ArticleMolecular psychiatry2014

Revisiting DARPP-32 in postmortem human brain: changes in schizophrenia and bipolar disorder and genetic associations with t-DARPP-32 expression.

Y Kunii, T M Hyde, T Ye, C Li, B Kolachana, D Dickinson, D R Weinberger, J E Kleinman, B K Lipska

Open access · bronzeAbstract read
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In one paragraph

Article in Molecular psychiatry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
3.7field-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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 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

9 authors at 2 institutions in 2 countries.

Y Kunii1] Section on Neuropathology, Clinical Brain Disorders Branch, Genes Cognition and Psychosis Program, Division of Intramural Research Programs, National Institute of Mental Health, Bethesda, MD, USA [2] Department of Neuropsychiatry, Fukushima Medical University School of Medicine, Fukushima, Japan.
T M Hyde1] Section on Neuropathology, Clinical Brain Disorders Branch, Genes Cognition and Psychosis Program, Division of Intramural Research Programs, National Institute of Mental Health, Bethesda, MD, USA [2] Lieber Institute for Brain Development, Johns Hopkins Medical Campus, Baltimore, MD, USA.
T Ye1] Section on Neuropathology, Clinical Brain Disorders Branch, Genes Cognition and Psychosis Program, Division of Intramural Research Programs, National Institute of Mental Health, Bethesda, MD, USA [2] Lieber Institute for Brain Development, Johns Hopkins Medical Campus, Baltimore, MD, USA.
C LiSection on Neuropathology, Clinical Brain Disorders Branch, Genes Cognition and Psychosis Program, Division of Intramural Research Programs, National Institute of Mental Health, Bethesda, MD, USA.
B KolachanaSection on Neuropathology, Clinical Brain Disorders Branch, Genes Cognition and Psychosis Program, Division of Intramural Research Programs, National Institute of Mental Health, Bethesda, MD, USA.
D DickinsonSection on Neuropathology, Clinical Brain Disorders Branch, Genes Cognition and Psychosis Program, Division of Intramural Research Programs, National Institute of Mental Health, Bethesda, MD, USA.
D R Weinberger1] Section on Neuropathology, Clinical Brain Disorders Branch, Genes Cognition and Psychosis Program, Division of Intramural Research Programs, National Institute of Mental Health, Bethesda, MD, USA [2] Lieber Institute for Brain Development, Johns Hopkins Medical Campus, Baltimore, MD, USA.
J E KleinmanSection on Neuropathology, Clinical Brain Disorders Branch, Genes Cognition and Psychosis Program, Division of Intramural Research Programs, National Institute of Mental Health, Bethesda, MD, USA.
B K LipskaSection on Neuropathology, Clinical Brain Disorders Branch, Genes Cognition and Psychosis Program, Division of Intramural Research Programs, National Institute of Mental Health, Bethesda, MD, USA.
Johns Hopkins University · USFukushima Medical University · JP

Funding

Procurement and Characterization of Postmortem Brain TissueZICMH002903 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI MARENCO, STEFANO · 2009 to 2025
$56.0M
Genetic Basis Of Cortical Malfunction In SchizophreniaZIAMH002734 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI BERMAN, KAREN FAITH · 2009 to 2014
$17.5M
Postmortem Brain Tissue Examination in Neuropsychiatric DisordersZIAMH002399 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI AMARA, SUSAN · 2009 to 2014
$11.9M
Characterization Of Neuropsychological Impairment In SchizophreniaZIAMH002712 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI BERMAN, KAREN FAITH · 2009 to 2014
$3.9M
Intramural NIH HHS
6 · The paper itself

Abstract

Dopamine- and cAMP-regulated phosphoprotein of molecular weight 32 kDa (DARPP-32 or PPP1R1B) has been of interest in schizophrenia owing to its critical function in integrating dopaminergic and glutaminergic signaling. In a previous study, we identified single-nucleotide polymorphisms (SNPs) and a frequent haplotype associated with cognitive and imaging phenotypes that have been linked with schizophrenia, as well as with expression of prefrontal cortical DARPP-32 messenger RNA (mRNA) in a relatively small sample of postmortem brains. In this study, we examined the association of expression of two major DARPP-32 transcripts, full-length (FL-DARPP-32) and truncated (t-DARPP-32), with genetic variants of DARPP-32 in three brain regions receiving dopaminergic input and implicated in schizophrenia (the dorsolateral prefrontal cortex (DLPFC), hippocampus and caudate) in a much larger set of postmortem samples from patients with schizophrenia, bipolar disorder, major depression and normal controls (>700 subjects). We found that the expression of t-DARPP-32 was increased in the DLPFC of patients with schizophrenia and bipolar disorder, and was strongly associated with genotypes at SNPs (rs879606, rs90974 and rs3764352), as well as the previously identified 7-SNP haplotype related to cognitive functioning. The genetic variants that predicted worse cognitive performance were associated with higher t-DARPP-32 expression. Our results suggest that variation in PPP1R1B affects the abundance of the splice variant t-DARPP-32 mRNA and may reflect potential molecular mechanisms implicated in schizophrenia and affective disorders.

Indexed as

AdolescentAdultAgedAged, 80 and overAnimalsAntipsychotic AgentsBipolar DisorderBrainChildChild, PreschoolDopamine and cAMP-Regulated Phosphoprotein 32FemaleFetusHumansInfantMajor Depressive DisorderAntipsychotic AgentsDopamine and cAMP-Regulated Phosphoprotein 32PPP1R1B protein, human

Identifiers

PMID23295814
OpenAlexW2001275516

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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.