Evidence map›Paper›PMID 29759351›Full record

ArticleSchizophrenia research2018

Dysbindin-1 contributes to prefrontal cortical dendritic arbor pathology in schizophrenia.

Glenn T Konopaske, Darrick T Balu, Kendall T Presti, Grace Chan, Francine M Benes, Joseph T Coyle

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Schizophrenia research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.1field-weighted citation impact, top 27% 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

10 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
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  10. Genetic polymorphism and neuroanatomical changes in schizophrenia.Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie
    Review
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

6 authors at 3 institutions in 1 country.

Glenn T KonopaskeMailman Research Center, McLean Hospital, Belmont, MA, USA; Department of Psychiatry, Harvard Medical School, Boston, MA, USA; Department of Psychiatry, University of Connecticut School of Medicine, Farmington, CT, USA. Electronic address: Konopaske@uchc.edu.
Darrick T BaluMailman Research Center, McLean Hospital, Belmont, MA, USA; Department of Psychiatry, Harvard Medical School, Boston, MA, USA.
Kendall T PrestiMailman Research Center, McLean Hospital, Belmont, MA, USA.
Grace ChanDepartment of Psychiatry, University of Connecticut School of Medicine, Farmington, CT, USA.
Francine M BenesMailman Research Center, McLean Hospital, Belmont, MA, USA; Department of Psychiatry, Harvard Medical School, Boston, MA, USA.
Joseph T CoyleMailman Research Center, McLean Hospital, Belmont, MA, USA; Department of Psychiatry, Harvard Medical School, Boston, MA, USA.
Harvard University · USMcLean Hospital · USUniversity of Connecticut · US

Funding

Molecular regulation of dendritic spines in schizophreniaK08MH087640 · NIMH · MCLEAN HOSPITAL · PI KONOPASKE, GLENN THOMAS · 2011 to 2015
$848k
NMDA receptor hypofunction contributes to the dendritic dysplasia in schizophreniR00MH099252 · NIMH · MCLEAN HOSPITAL · PI BALU, DARRICK T · 2015 to 2017
$726k
NMDA receptor hypofunction contributes to the dendritic dysplasia in schizophreniK99MH099252 · NIMH · MCLEAN HOSPITAL · PI BALU, DARRICK T · 2013 to 2014
$230k
NIMH NIH HHS K08 MH087640NIMH NIH HHS K99 MH099252NIMH NIH HHS R00 MH099252
6 · The paper itself

Abstract

Deep layer III pyramidal cells in the dorsolateral prefrontal cortex (DLPFC) from subjects with schizophrenia and bipolar disorder previously were shown to exhibit dendritic arbor pathology. This study sought to determine whether MARCKS, its regulatory protein dysbindin-1, and two proteins, identified using microarray data, CDC42BPA and ARHGEF6, were associated with dendritic arbor pathology in the DLPFC from schizophrenia and bipolar disorder subjects. Using western blotting, relative protein expression was assessed in the DLPFC (BA 46) grey matter from subjects with schizophrenia (n = 19), bipolar disorder (n = 17) and unaffected control subjects (n = 19). Protein expression data were then correlated with dendritic parameter data obtained previously. MARCKS and dysbindin-1a expression levels did not differ among the three groups. Dysbindin-1b expression was 26% higher in schizophrenia subjects (p = 0.01) and correlated inversely with basilar dendrite length (r = -0.31, p = 0.048) and the number of spines per basilar dendrite (r = -0.31, p = 0.048), but not with dendritic spine density (r = -0.16, p = 0.32). The protein expression of CDC42BPA was 33% higher in schizophrenia subjects (p = 0.03) but, did not correlate with any dendritic parameter (p > 0.05). ARHGEF6 87 kDa isoform expression did not differ among the groups. CDC42BPA expression was not altered in frontal cortex from rats chronically administered haloperidol or clozapine. Dysbindin-1b appears to play a role in dendritic arbor pathology observed previously in the DLPFC in schizophrenia.

Indexed as

AnimalsBipolar DisorderCohort StudiesDendritesDisease Models, AnimalDysbindinFemaleGene ExpressionGray MatterHumansMaleMiddle AgedMyotonin-Protein KinaseMyristoylated Alanine-Rich C Kinase SubstratePrefrontal CortexProtein IsoformsARHGEF6 protein, humanCDC42BPA protein, humanCdc42bpa protein, ratDTNBP1 protein, humanDysbindinMARCKS protein, humanMyotonin-Protein KinaseMyristoylated Alanine-Rich C Kinase SubstrateProtein IsoformsProtein Serine-Threonine KinasesPsychotropic DrugsRho Guanine Nucleotide Exchange FactorsBipolar disorderDendriteDysbindin-1PostmortemSchizophreniaWestern blot

Identifiers

PMID29759351
PMCPMC6230503
OpenAlexW2800912535

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.