Evidence map›Paper›PMID 27598967›Full record

ArticleTranslational psychiatry2016

Genome-wide association study of antisocial personality disorder.

M-R Rautiainen, T Paunio, E Repo-Tiihonen, M Virkkunen, H M Ollila, S Sulkava, O Jolanki, A Palotie, J Tiihonen

Open access · goldAbstract read
In one paragraph

Article in Translational psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
11.5field-weighted citation impact, top 1% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Aggression based genome-wide, glutamatergic, dopaminergic and neuroendocrine polygenic risk scores predict callous-unemotional traits.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020
    Article
  9. Review
  10. Article
  11. Review
  12. Molecular neuropsychiatry · 2018
    Review
  13. Article
  14. SALM/Lrfn Family Synaptic Adhesion Molecules.Frontiers in molecular neuroscience · 2018
    Review
  15. Article
  16. 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

9 authors at 6 institutions in 4 countries.

M-R RautiainenNational Institute for Health and Welfare, Department of Health, Helsinki, Finland.
T PaunioNational Institute for Health and Welfare, Department of Health, Helsinki, Finland.
E Repo-TiihonenDepartment of Forensic Psychiatry, Niuvanniemi Hospital, University of Eastern Finland, Kuopio, Finland.
M VirkkunenDepartment of Psychiatry, University of Helsinki, Helsinki, Finland.
H M OllilaNational Institute for Health and Welfare, Department of Health, Helsinki, Finland.
S SulkavaNational Institute for Health and Welfare, Department of Health, Helsinki, Finland.
O JolankiStanford University Center for Sleep Sciences, Palo Alto, CA, USA.
A PalotieInstitute for Molecular Medicine Finland, University of Helsinki, Helsinki, Finland.
J TiihonenDepartment of Forensic Psychiatry, Niuvanniemi Hospital, University of Eastern Finland, Kuopio, Finland.
Finnish Institute for Health and Welfare · FIHelsinki University Hospital · FIInstitute for Molecular Medicine Finland · FINiuvanniemi Hospital · FIStanford University · USUniversity of Eastern Finland · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pathophysiology of antisocial personality disorder (ASPD) remains unclear. Although the most consistent biological finding is reduced grey matter volume in the frontal cortex, about 50% of the total liability to developing ASPD has been attributed to genetic factors. The contributing genes remain largely unknown. Therefore, we sought to study the genetic background of ASPD. We conducted a genome-wide association study (GWAS) and a replication analysis of Finnish criminal offenders fulfilling DSM-IV criteria for ASPD (N=370, N=5850 for controls, GWAS; N=173, N=3766 for controls and replication sample). The GWAS resulted in suggestive associations of two clusters of single-nucleotide polymorphisms at 6p21.2 and at 6p21.32 at the human leukocyte antigen (HLA) region. Imputation of HLA alleles revealed an independent association with DRB1*01:01 (odds ratio (OR)=2.19 (1.53-3.14), P=1.9 × 10(-5)). Two polymorphisms at 6p21.2 LINC00951-LRFN2 gene region were replicated in a separate data set, and rs4714329 reached genome-wide significance (OR=1.59 (1.37-1.85), P=1.6 × 10(-9)) in the meta-analysis. The risk allele also associated with antisocial features in the general population conditioned for severe problems in childhood family (β=0.68, P=0.012). Functional analysis in brain tissue in open access GTEx and Braineac databases revealed eQTL associations of rs4714329 with LINC00951 and LRFN2 in cerebellum. In humans, LINC00951 and LRFN2 are both expressed in the brain, especially in the frontal cortex, which is intriguing considering the role of the frontal cortex in behavior and the neuroanatomical findings of reduced gray matter volume in ASPD. To our knowledge, this is the first study showing genome-wide significant and replicable findings on genetic variants associated with any personality disorder.

Indexed as

AdultAntisocial Personality DisorderBrainCase-Control StudiesCell Adhesion MoleculesCerebellumChromosomes, Human, Pair 6CriminalsFemaleFinlandFrontal LobeGenome-Wide Association StudyGray MatterHLA AntigensHLA-DR alpha-ChainsHLA-DRB1 ChainsCell Adhesion MoleculesHLA AntigensHLA-DR alpha-ChainsHLA-DRB1*01:01 antigenHLA-DRB1 ChainsLRFN2 protein, humanMembrane GlycoproteinsMembrane ProteinsNerve Tissue ProteinsRNA, Long NoncodingSDK1 protein, human

Identifiers

PMID27598967
PMCPMC5048197
OpenAlexW2514744061

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.