Evidence map›Paper›PMID 21901269›Full record

ArticleEuropean archives of psychiatry and clinical neuroscience2012

A promoter variant of SHANK1 affects auditory working memory in schizophrenia patients and in subjects clinically at risk for psychosis.

Leonhard Lennertz, Michael Wagner, Wolfgang Wölwer, Anna Schuhmacher, Ingo Frommann, Julia Berning, Svenja Schulze-Rauschenbach, Martin W Landsberg, Anja Steinbrecher, Michael Alexander and 9 more

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In one paragraph

Article in European archives of psychiatry and clinical neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.1field-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

14 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
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  4. Review
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  7. Synapse assembly and neurodevelopmental disorders.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2015
    Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Neurobiology of schizophrenia: from outcome to pathophysiological insights.European archives of psychiatry and clinical neuroscience · 2012
    Article
  14. 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

19 authors at 5 institutions in 1 country.

Leonhard LennertzDepartment of Psychiatry and Psychotherapy, University of Bonn, Sigmund-Freud-Straße 25, 53105, Bonn, Germany.
Michael Wagner
Wolfgang Wölwer
Anna Schuhmacher
Ingo Frommann
Julia Berning
Svenja Schulze-Rauschenbach
Martin W Landsberg
Anja Steinbrecher
Michael Alexander
Petra E Franke
Ralf Pukrop
Stephan Ruhrmann
Andreas Bechdolf
Wolfgang Gaebel
Joachim Klosterkötter
Heinz Häfner
Wolfgang Maier
Rainald Mössner
University of Bonn · DEUniversity of Cologne · DEHeinrich Heine University Düsseldorf · DECentral Institute of Mental Health · DELife & Brain (Germany) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mutations in postsynaptic scaffolding genes contribute to autism, thus suggesting a role in pathological processes in neurodevelopment. Recently, two de novo mutations in SHANK3 were described in schizophrenia patients. In most cases, abnormal SHANK3 genotype was also accompanied by cognitive disruptions. The present study queries whether common SHANK variants may also contribute to neuropsychological dysfunctions in schizophrenia. We genotyped five common coding or promoter variants located in SHANK1, SHANK2 and SHANK3. A comprehensive test battery was used to assess neuropsychological functions in 199 schizophrenia patients and 206 healthy control subjects. In addition, an independent sample of 77 subjects at risk for psychosis was analyzed for replication of significant findings. We found the T allele of the SHANK1 promoter variant rs3810280 to lead to significantly impaired auditory working memory as assessed with digit span (12.5 ± 3.6 vs. 14.8 ± 4.1, P < .001) in schizophrenia cases, applying strict Bonferroni correction for multiple testing. This finding was replicated for forward digit span in the at-risk sample (7.1 ± 2.0 vs. 8.3 ± 2.0, P = .044). Previously, altered memory functions and reduced dendritic spines and postsynaptic density of excitatory synapses were reported in SHANK1 knock-out mice. Moreover, the atypical neuroleptic clozapine was found to increase SHANK1 density in rats. Our findings suggest a role of SHANK1 in working memory deficits in schizophrenia, which may arise from neurodevelopmental changes to prefrontal cortical areas.

Indexed as

Acoustic StimulationAdaptor Proteins, Signal TransducingAdultAgedFemaleGenotypeHumansMaleMemory DisordersMemory, Short-TermMiddle AgedNerve Tissue ProteinsNeuropsychological TestsPromoter Regions, GeneticPsychiatric Status Rating ScalesPsychotic DisordersAdaptor Proteins, Signal TransducingNerve Tissue ProteinsShank1 protein, rat

Identifiers

PMID21901269
OpenAlexW2149947428

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.