Evidence map›Paper›PMID 22539971›Full record

ArticlePloS one2012

DCLK1 variants are associated across schizophrenia and attention deficit/hyperactivity disorder.

Bjarte Håvik, Franziska A Degenhardt, Stefan Johansson, Carla P D Fernandes, Anke Hinney, André Scherag, Helle Lybæk, Srdjan Djurovic, Andrea Christoforou, Kari M Ersland and 22 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.5field-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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Detecting and treating adult attention deficit hyperactivity disorder in a patient with schizophrenia.Neuropsychiatrie : Klinik, Diagnostik, Therapie und Rehabilitation : Organ der Gesellschaft Osterreichischer Nervenarzte und Psychiater · 2014
    Article
  17. 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

32 authors at 11 institutions in 4 countries.

Bjarte HåvikDr E Martens Research Group for Biological Psychiatry, Department of Clinical Medicine, University of Bergen, Bergen, Norway.
Franziska A Degenhardt
Stefan Johansson
Carla P D Fernandes
Anke Hinney
André Scherag
Helle Lybæk
Srdjan Djurovic
Andrea Christoforou
Kari M Ersland
Sudheer Giddaluru
Michael C O'Donovan
Michael J Owen
Nick Craddock
Thomas W Mühleisen
Manuel Mattheisen
Benno G Schimmelmann
Tobias Renner
Andreas Warnke
Beate Herpertz-Dahlmann
Judith Sinzig
Özgür Albayrak
Marcella Rietschel
Markus M Nöthen
Clive R Bramham
Thomas Werge
Johannes Hebebrand
Jan Haavik
Ole A Andreassen
Sven Cichon
Vidar M Steen
Stéphanie Le Hellard
University of Bergen · NOUniversity of Duisburg-Essen · DECardiff University · GBHaukeland University Hospital · NOLife & Brain (Germany) · DEUniversity of Bonn · DEUniversity of Würzburg · DECopenhagen University Hospital · DKLVR-Klinik Bonn · DEOslo University Hospital · NOUniversity of Oslo · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Doublecortin and calmodulin like kinase 1 (DCLK1) is implicated in synaptic plasticity and neurodevelopment. Genetic variants in DCLK1 are associated with cognitive traits, specifically verbal memory and general cognition. We investigated the role of DCLK1 variants in three psychiatric disorders that have neuro-cognitive dysfunctions: schizophrenia (SCZ), bipolar affective disorder (BP) and attention deficit/hyperactivity disorder (ADHD). We mined six genome wide association studies (GWASs) that were available publically or through collaboration; three for BP, two for SCZ and one for ADHD. We also genotyped the DCLK1 region in additional samples of cases with SCZ, BP or ADHD and controls that had not been whole-genome typed. In total, 9895 subjects were analysed, including 5308 normal controls and 4,587 patients (1,125 with SCZ, 2,496 with BP and 966 with ADHD). Several DCLK1 variants were associated with disease phenotypes in the different samples. The main effect was observed for rs7989807 in intron 3, which was strongly associated with SCZ alone and even more so when cases with SCZ and ADHD were combined (P-value = 4 × 10(-5) and 4 × 10(-6), respectively). Associations were also observed with additional markers in intron 3 (combination of SCZ, ADHD and BP), intron 19 (SCZ+BP) and the 3'UTR (SCZ+BP). Our results suggest that genetic variants in DCLK1 are associated with SCZ and, to a lesser extent, with ADHD and BP. Interestingly the association is strongest when SCZ and ADHD are considered together, suggesting common genetic susceptibility. Given that DCLK1 variants were previously found to be associated with cognitive traits, these results are consistent with the role of DCLK1 in neurodevelopment and synaptic plasticity.

Indexed as

Attention Deficit Disorder with HyperactivityBipolar DisorderDoublecortin-Like KinasesGenetic Predisposition to DiseaseGenome-Wide Association StudyGenotypeHumansIntracellular Signaling Peptides and ProteinsIntronsOdds RatioPhenotypePolymorphism, Single NucleotideProtein Serine-Threonine KinasesSchizophreniaDCLK1 protein, humanDoublecortin-Like KinasesIntracellular Signaling Peptides and ProteinsProtein Serine-Threonine Kinases

Identifiers

PMID22539971
PMCPMC3335166
OpenAlexW1991979830

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.