Evidence map›Paper›PMID 25801500›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2015

NCAN Cross-Disorder Risk Variant Is Associated With Limbic Gray Matter Deficits in Healthy Subjects and Major Depression.

Udo Dannlowski, Harald Kugel, Dominik Grotegerd, Ronny Redlich, Janina Suchy, Nils Opel, Thomas Suslow, Carsten Konrad, Patricia Ohrmann, Jochen Bauer and 13 more

Open access · bronzeAbstract read
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 5 pooled it
2.7field-weighted citation impact, top 10% 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

13 citing papers in PubMed, 5 syntheses or guidelines pooled it, 62 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. The neuroanatomy of depression: weak but replicable effects in 4021 individuals from three clinical cohorts.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Article
  7. Article
  8. Biological sex classification with structural MRI data shows increased misclassification in transgender women.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020
    Article
  9. Article
  10. Article
  11. Further Evidence of an Association betweenMolecular neuropsychiatry · 2018
    Article
  12. Article
  13. TheNeuropsychiatric disease and treatment · 2016
    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

23 authors at 8 institutions in 2 countries.

Udo DannlowskiDepartment of Psychiatry, University of Marburg, Marburg, Germany.
Harald KugelDepartment of Clinical Radiology, University of Münster, Münster, Germany.
Dominik GrotegerdDepartment of Psychiatry, University of Münster, Münster, Germany.
Ronny RedlichDepartment of Psychiatry, University of Münster, Münster, Germany.
Janina SuchyDepartment of Psychiatry, University of Münster, Münster, Germany.
Nils OpelDepartment of Psychiatry, University of Münster, Münster, Germany.
Thomas SuslowDepartment of Psychosomatic Medicine, University of Leipzig, Leipzig, Germany.
Carsten KonradDepartment of Psychiatry, University of Marburg, Marburg, Germany.
Patricia OhrmannDepartment of Psychiatry, University of Münster, Münster, Germany.
Jochen BauerDepartment of Psychiatry, University of Münster, Münster, Germany.
Tilo KircherDepartment of Psychiatry, University of Marburg, Marburg, Germany.
Axel KrugDepartment of Psychiatry, University of Marburg, Marburg, Germany.
Andreas JansenDepartment of Psychiatry, University of Marburg, Marburg, Germany.
Bernhard T BauneDiscipline of Psychiatry, School of Medicine, University of Adelaide, Adelaide, SA, Australia.
Walter HeindelDepartment of Clinical Radiology, University of Münster, Münster, Germany.
Katharina DomschkeDepartment of Psychiatry, University of Würzburg, Würzburg, Germany.
Andreas J ForstnerInstitute of Human Genetics, University of Bonn, Bonn, Germany.
Markus M NöthenInstitute of Human Genetics, University of Bonn, Bonn, Germany.
Jens TreutleinDepartment of Genetic Epidemiology in Psychiatry, Central Institute of Mental Health, Mannheim, Germany.
Volker AroltDepartment of Psychiatry, University of Münster, Münster, Germany.
Christa HohoffDepartment of Psychiatry, University of Münster, Münster, Germany.
Marcella RietschelDepartment of Genetic Epidemiology in Psychiatry, Central Institute of Mental Health, Mannheim, Germany.
Stephanie H WittDepartment of Genetic Epidemiology in Psychiatry, Central Institute of Mental Health, Mannheim, Germany.
University of Münster · DEPhilipps University of Marburg · DECentral Institute of Mental Health · DELeipzig University · DELife & Brain (Germany) · DEUniversity of Adelaide · AUUniversity of Bonn · DEUniversity of Würzburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genome-wide association studies have reported an association between NCAN rs1064395 genotype and bipolar disorder. This association was later extended to schizophrenia and major depression. However, the neurobiological underpinnings of these associations are poorly understood. NCAN is implicated in neuronal plasticity and expressed in subcortical brain areas, such as the amygdala and hippocampus, which are critically involved in dysfunctional emotion processing and regulation across diagnostic boundaries. We hypothesized that the NCAN risk variant is associated with reduced gray matter volumes in these areas. Gray matter structure was assessed by voxel-based morphometry on structural MRI data in two independent German samples (healthy subjects, n=512; depressed inpatients, n=171). All participants were genotyped for NCAN rs1064395. Hippocampal and amygdala region-of-interest analyses were performed within each sample. In addition, whole-brain data from the combined sample were analyzed. Risk (A)-allele carriers showed reduced amygdala and hippocampal gray matter volumes in both cohorts with a remarkable spatial overlap. In the combined sample, genotype effects observed for the amygdala and hippocampus survived correction for entire brain volume. Further effects were also observed in the left orbitofrontal cortex and the cerebellum/fusiform gyrus. We conclude that NCAN genotype is associated with limbic gray matter alterations in healthy and depressed subjects in brain areas implicated in emotion perception and regulation. The present data suggest that NCAN forms susceptibility to neurostructural deficits in the amygdala, hippocampus, and prefrontal areas independent of disease, which might lead to disorder onset in the presence of other genetic or environmental risk factors.

Indexed as

AdolescentAdultAgedBipolar DisorderChondroitin Sulfate ProteoglycansCohort StudiesFemaleGenetic Association StudiesGenetic Predisposition to DiseaseGenetic VariationGenotyping TechniquesGray MatterHumansInpatientsLectins, C-TypeLimbic SystemChondroitin Sulfate ProteoglycansLectins, C-TypeNCAN protein, humanNerve Tissue ProteinsNeurocan

Identifiers

PMID25801500
PMCPMC4569958
OpenAlexW2088266958

What OpenQuestion holds

Textmetadata
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.