Evidence map›Paper›PMID 25517604›Full record

ArticlePloS one2014

A genetic variant in 12q13, a possible risk factor for bipolar disorder, is associated with depressive state, accounting for stressful life events.

Ayu Shimasaki, Kenji Kondo, Takeo Saito, Kosei Esaki, Yasuyo Otsuka, Keiko Mano, Masashi Ikeda, Nakao Iwata

Open access · goldAbstract readComparative Study
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

6 citing papers in PubMed, 13 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Ayu ShimasakiDepartment of Psychiatry, Fujita Health University School of Medicine, Toyoake, Aichi, Japan.
Kenji KondoDepartment of Psychiatry, Fujita Health University School of Medicine, Toyoake, Aichi, Japan.
Takeo SaitoDepartment of Psychiatry, Fujita Health University School of Medicine, Toyoake, Aichi, Japan.
Kosei EsakiDepartment of Psychiatry, Fujita Health University School of Medicine, Toyoake, Aichi, Japan.
Yasuyo OtsukaDivision of Nursing, Fujita Health University Hospital, Toyoake, Aichi, Japan.
Keiko ManoDivision of Nursing, Fujita Health University Hospital, Toyoake, Aichi, Japan.
Masashi IkedaDepartment of Psychiatry, Fujita Health University School of Medicine, Toyoake, Aichi, Japan.
Nakao IwataDepartment of Psychiatry, Fujita Health University School of Medicine, Toyoake, Aichi, Japan.
Fujita Health University · JPFujita Health University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genome-wide association studies (GWASs) have identified a number of susceptibility genes for schizophrenia (SCZ) and bipolar disorder (BD). However, the identification of risk genes for major depressive disorder (MDD) has been unsuccessful because the etiology of MDD is more influenced by environmental factors; thus, gene-environment (G × E) interactions are important, such as interplay with stressful life events (SLEs). We assessed the G×E interactions and main effects of genes targeting depressive symptoms. Using a case-control design, 922 hospital staff members were evaluated for depressive symptoms according to Beck Depressive Inventory (BDI; "depression" and "control" groups were classified by scores of 10 in the BDI test), SLEs, and personality. A total of sixty-three genetic variants were selected on the basis of previous GWASs of MDD, SCZ, and BD as well as candidate-gene (SLC6A4, BDNF, DBH, and FKBP5) studies. Logistic regression analysis revealed a marginally significant interaction (genetic variant × SLE) at rs4523957 (P uncorrected = 0.0034) with depression and a significant association of single nucleotide polymorphism identified from evidence of BD GWAS (rs7296288, downstream of DHH at 12q13.1) with depression as the main effect (P uncorrected = 9.4 × 10(-4), P corrected = 0.0424). We also found that SLEs had a larger impact on depression (odds ratio ∼ 3), as reported previously. These results suggest that DHH plays a possible role in depression etiology; however, variants from MDD or SCZ GWAS evidence or candidate genes showed no significant associations or minimal effects of interactions with SLEs on depression.

Indexed as

Life Change EventsAdultBiomarkersBipolar DisorderCase-Control StudiesChromosomes, Human, Pair 12FemaleFollow-Up StudiesGene-Environment InteractionGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansJapanMajor Depressive DisorderMaleMiddle AgedBiomarkers

Identifiers

PMID25517604
PMCPMC4269417
OpenAlexW2047534429

What OpenQuestion holds

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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.