Evidence map›Paper›PMID 28117839›Full record

SynthesisTranslational psychiatry2017

The genetic overlap between mood disorders and cardiometabolic diseases: a systematic review of genome wide and candidate gene studies.

A T Amare, K O Schubert, M Klingler-Hoffmann, S Cohen-Woods, B T Baune

Open access · goldAbstract readSystematic Review
PubMed Full text at PMC Publisher
In one paragraph

Synthesis in Translational psychiatry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 148 papers, 10 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
148citing papers in PubMed, 10 pooled it
24.9field-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

148 citing papers in PubMed, 10 syntheses or guidelines pooled it, 342 citations in OpenAlex.

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88 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

A T AmareDiscipline of Psychiatry, School of Medicine, The University of Adelaide, Adelaide, SA, Australia.
K O SchubertDiscipline of Psychiatry, School of Medicine, The University of Adelaide, Adelaide, SA, Australia.
M Klingler-HoffmannAdelaide Proteomics Centre, School of Biological Sciences, The University of Adelaide, Adelaide, SA, Australia.
S Cohen-WoodsSchool of Psychology, Faculty of Social and Behavioural Sciences, Flinders University, Adelaide, SA, Australia.
B T BauneDiscipline of Psychiatry, School of Medicine, The University of Adelaide, Adelaide, SA, Australia.
University of Adelaide · AUFlinders University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Meta-analyses of genome-wide association studies (meta-GWASs) and candidate gene studies have identified genetic variants associated with cardiovascular diseases, metabolic diseases and mood disorders. Although previous efforts were successful for individual disease conditions (single disease), limited information exists on shared genetic risk between these disorders. This article presents a detailed review and analysis of cardiometabolic diseases risk (CMD-R) genes that are also associated with mood disorders. First, we reviewed meta-GWASs published until January 2016, for the diseases 'type 2 diabetes, coronary artery disease, hypertension' and/or for the risk factors 'blood pressure, obesity, plasma lipid levels, insulin and glucose related traits'. We then searched the literature for published associations of these CMD-R genes with mood disorders. We considered studies that reported a significant association of at least one of the CMD-R genes and 'depression' or 'depressive disorder' or 'depressive symptoms' or 'bipolar disorder' or 'lithium treatment response in bipolar disorder', or 'serotonin reuptake inhibitors treatment response in major depression'. Our review revealed 24 potential pleiotropic genes that are likely to be shared between mood disorders and CMD-Rs. These genes include MTHFR, CACNA1D, CACNB2, GNAS, ADRB1, NCAN, REST, FTO, POMC, BDNF, CREB, ITIH4, LEP, GSK3B, SLC18A1, TLR4, PPP1R1B, APOE, CRY2, HTR1A, ADRA2A, TCF7L2, MTNR1B and IGF1. A pathway analysis of these genes revealed significant pathways: corticotrophin-releasing hormone signaling, AMPK signaling, cAMP-mediated or G-protein coupled receptor signaling, axonal guidance signaling, serotonin or dopamine receptors signaling, dopamine-DARPP32 feedback in cAMP signaling, circadian rhythm signaling and leptin signaling. Our review provides insights into the shared biological mechanisms of mood disorders and cardiometabolic diseases.

Indexed as

Antimanic AgentsBipolar DisorderBlood PressureCoronary Artery DiseaseDepressionDiabetes Mellitus, Type 2Genome-Wide Association StudyGlucoseHumansHypertensionInsulinLipid MetabolismLithium CompoundsMajor Depressive DisorderObesitySelective Serotonin Reuptake InhibitorsAntimanic AgentsGlucoseInsulinLithium CompoundsSelective Serotonin Reuptake Inhibitors

Identifiers

PMID28117839
PMCPMC5545727
OpenAlexW2949712093

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.