Evidence map›Paper›PMID 31385059›Full record

ArticleInternational journal of bipolar disorders2019

Epigenetic markers in inflammation-related genes associated with mood disorder: a cross-sectional and longitudinal study in high-risk offspring of bipolar parents.

Anne Duffy, Sarah M Goodday, Charles Keown-Stoneman, Martina Scotti, Malosree Maitra, Corina Nagy, Julie Horrocks, Gustavo Turecki

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In one paragraph

Article in International journal of bipolar disorders, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

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

  1. Pooled it
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  7. DNA methylation in blood cells is associated with cortisol levels in offspring of mothers who had prenatal post-traumatic stress disorder.Stress and health : journal of the International Society for the Investigation of Stress · 2022
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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.

Anne DuffyDivision of Student Mental Health, Department of Psychiatry, Queen's University, 146 Stuart Street, Kingston, ON, Canada. anne.duffy@queensu.ca.ORCID http://orcid.org/0000-0002-5895-075X
Sarah M GooddayDepartment of Psychiatry, University of Oxford, Oxford, UK.
Charles Keown-StonemanDalla Lana School of Public Health, University of Toronto, Toronto, ON, Canada.
Martina ScottiMcGill Group for Suicide Studies, Department of Psychiatry, Douglas Institute, McGill University, Montreal, QC, Canada.
Malosree MaitraMcGill Group for Suicide Studies, Department of Psychiatry, Douglas Institute, McGill University, Montreal, QC, Canada.
Corina NagyMcGill Group for Suicide Studies, Department of Psychiatry, Douglas Institute, McGill University, Montreal, QC, Canada.
Julie HorrocksDepartment of Mathematics and Statistics, Guelph University, Guelph, ON, Canada.
Gustavo TureckiMcGill Group for Suicide Studies, Department of Psychiatry, Douglas Institute, McGill University, Montreal, QC, Canada.

Funding

Canadian Institutes of Health Research 152976Hotchkiss Brain Institute, Calgary, Alberta (CA) Pilot Research Fund 2014
6 · The paper itself

Abstract

Bipolar disorder is highly heritable and typically onsets in late adolescence or early adulthood. Evidence suggests that immune activation may be a mediating pathway between genetic predisposition and onset of mood disorders. Building on a prior study of mRNA and protein levels in high-risk offspring published in this Journal, we conducted a preliminary examination of methylation profiles in candidate immune genes from a subsample of well-characterized emergent adult (mean 20 years) offspring of bipolar parents from the Canadian Flourish high-risk cohort. Models were adjusted for variable age at DNA collection, sex and antidepressant and mood stabilizer use. On cross-sectional analysis, there was evidence of higher methylation rates for BDNF-1 in high-risk offspring affected (n = 27) and unaffected (n = 23) for mood disorder compared to controls (n = 24) and higher methylation rates in affected high-risk offspring for NR3C1 compared to controls. Longitudinal analyses (25 to 34 months) provided evidence of steeper decline in methylation rates in controls (n = 24) for NR3C1 compared to affected (n = 15) and unaffected (n = 11) high-risk offspring and for BDNF-2 compared to affected high-risk. There was insufficient evidence that changes in any of the candidate gene methylation rates were associated with illness recurrence in high-risk offspring. While preliminary, findings suggest that longitudinal investigation of epigenetic markers in well-characterized high-risk individuals over the peak period of risk may be informative to understand the emergence of bipolar disorder.

Indexed as

Bipolar disorderCross-sectionalEpigenetic markersHigh-risk offspringInflammatory candidate genesLongitudinalMethylation profiles

Identifiers

PMID31385059
PMCPMC6682840

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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.