Evidence map›Paper›PMID 31559935›Full record

ReviewPsychological medicine2019

Unraveling the genetic architecture of major depressive disorder: merits and pitfalls of the approaches used in genome-wide association studies.

I Schwabe, Y Milaneschi, Z Gerring, P F Sullivan, E Schulte, N P Suppli, J G Thorp, E M Derks, C M Middeldorp

Abstract readReview
In one paragraph

Review in Psychological medicine, 2019. 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
–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

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

  1. Pooled it
  2. Article
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  4. Peripheral MicroRNA Signatures in Adolescent Depression.Biological psychiatry global open science · 2025
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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

9 authors.

I SchwabeDepartment of Methodology and Statistics, Tilburg University, Tilburg, The Netherlands.ORCID 0000-0002-3465-8308
Y MilaneschiDepartment of Psychiatry, Amsterdam Neuroscience and Amsterdam Public Health Research Institute, Amsterdam University Medical Center, Amsterdam, The Netherlands.
Z GerringTranslational Neurogenomics Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, Australia.
P F SullivanDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
E SchulteMedical Centre of the University of Munich, Munich, Germany.
N P SuppliMental Health Centre Copenhagen, Copenhagen University Hospital, Copenhagen, Denmark.
J G ThorpTranslational Neurogenomics Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, Australia.
E M DerksTranslational Neurogenomics Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, Australia.
C M MiddeldorpChild Health Research Centre, University of Queensland, Brisbane, Australia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To identify genetic risk loci for major depressive disorder (MDD), two broad study design approaches have been applied: (1) to maximize sample size by combining data from different phenotype assessment modalities (e.g. clinical interview, self-report questionnaires) and (2) to reduce phenotypic heterogeneity through selecting more homogenous MDD subtypes. The value of these strategies has been debated. In this review, we summarize the most recent findings of large genomic studies that applied these approaches, and we highlight the merits and pitfalls of both approaches with particular attention to methodological and psychometric issues. We also discuss the results of analyses that investigated the heterogeneity of MDD. We conclude that both study designs are essential for further research. So far, increasing sample size has led to the identification of a relatively high number of genomic loci linked to depression. However, part of the identified variants may be related to a phenotype common to internalizing disorders and related traits. As such, samples containing detailed clinical information are needed to dissect depression heterogeneity and enable the potential identification of variants specific to a more restricted MDD phenotype. A balanced portfolio reconciling both study design approaches is the optimal approach to progress further in unraveling the genetic architecture of depression.

Indexed as

Genetic Predisposition to DiseaseGenome-Wide Association StudyDepressionGenetic LociHumansMajor Depressive DisorderMultifactorial InheritancePhenotypePolymorphism, Single NucleotideRisk FactorsDepressionGWASMDDphenotypic heterogeneitypowerPRSpsychometrics

Identifiers

PMID31559935
PMCPMC6877467

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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.