Evidence map›Paper›PMID 27956746›Full record

ArticleMolecular psychiatry2017

Schizophrenia copy number variants and associative learning.

N E Clifton, A J Pocklington, B Scholz, E Rees, J T R Walters, G Kirov, M C O'Donovan, M J Owen, L S Wilkinson, K L Thomas and 1 more

Abstract read
In one paragraph

Article in Molecular psychiatry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
  4. Copy Number Variations and Schizophrenia.Molecular neurobiology · 2023
    Review
  5. Review
  6. Article
  7. Article
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  9. Article
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  11. Article
  12. Review
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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

11 authors.

N E CliftonNeuroscience and Mental Health Research Institute, Cardiff University, Cardiff, UK.
A J PocklingtonNeuroscience and Mental Health Research Institute, Cardiff University, Cardiff, UK.
B ScholzNeuroscience and Mental Health Research Institute, Cardiff University, Cardiff, UK.
E ReesMRC Centre for Neuropsychiatric Genetics and Genomics, Institute of Psychological Medicine and Clinical Neurosciences, Cardiff University, Cardiff, UK.
J T R WaltersMRC Centre for Neuropsychiatric Genetics and Genomics, Institute of Psychological Medicine and Clinical Neurosciences, Cardiff University, Cardiff, UK.
G KirovMRC Centre for Neuropsychiatric Genetics and Genomics, Institute of Psychological Medicine and Clinical Neurosciences, Cardiff University, Cardiff, UK.
M C O'DonovanNeuroscience and Mental Health Research Institute, Cardiff University, Cardiff, UK.
M J OwenNeuroscience and Mental Health Research Institute, Cardiff University, Cardiff, UK.
L S WilkinsonNeuroscience and Mental Health Research Institute, Cardiff University, Cardiff, UK.
K L ThomasNeuroscience and Mental Health Research Institute, Cardiff University, Cardiff, UK.
J HallNeuroscience and Mental Health Research Institute, Cardiff University, Cardiff, UK.

Funding

Medical Research Council G0801418Medical Research Council MR/L010305/1Medical Research Council MR/P005748/1Wellcome TrustWellcome Trust 100202/Z/12/Z
6 · The paper itself

Abstract

Large-scale genomic studies have made major progress in identifying genetic risk variants for schizophrenia. A key finding from these studies is that there is an increased burden of genomic copy number variants (CNVs) in schizophrenia cases compared with controls. The mechanism through which these CNVs confer risk for the symptoms of schizophrenia, however, remains unclear. One possibility is that schizophrenia risk CNVs impact basic associative learning processes, abnormalities of which have long been associated with the disorder. To investigate whether genes in schizophrenia CNVs impact on specific phases of associative learning we combined human genetics with experimental gene expression studies in animals. In a sample of 11 917 schizophrenia cases and 16 416 controls, we investigated whether CNVs from patients with schizophrenia are enriched for genes expressed during the consolidation, retrieval or extinction of associative memories. We show that CNVs from cases are enriched for genes expressed during fear extinction in the hippocampus, but not genes expressed following consolidation or retrieval. These results suggest that CNVs act to impair inhibitory learning in schizophrenia, potentially contributing to the development of core symptoms of the disorder.

Indexed as

AnimalsAssociation LearningCA1 Region, HippocampalCase-Control StudiesConditioning, ClassicalDatabases, FactualDNA Copy Number VariationsFearFemaleGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansMaleRatsSchizophrenia

Identifiers

PMID27956746
PMCPMC5285462

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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.