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Stress Hormone System and Epigenetics in Depression

Published online by Cambridge University Press:  23 March 2020

V. O’Keane
Affiliation:
Psychiatry, Ireland
C. Farrell
Affiliation:
Trinity college institute of neurosciences, psychiatry, Dublin, Ireland
K. Doolin
Affiliation:
TCIN, psychiatry, Dublin, Ireland
J. Chai
Affiliation:
TCIN, psychiatry, Dublin, Ireland
N. O’leary
Affiliation:
TCIN, psychology, Dublin, Ireland
T. Frodl
Affiliation:
Magdeburg university, universitätsklinik für psychiatrie und psychotherapie, Magdeburg, Ireland
L. Booji
Affiliation:
Psychology, Montreal, Canada
L. Tozzi
Affiliation:
TCIN, psychiatry, Dublin, Ireland

Abstract

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Background

Exposure to early life adversity (ELA) has been identified as a major risk factor in the development of major depressive disorder (MDD). It is hypothesized that a mediating mechanism may be environmentally induced alterations in gene function. In our REDEEM (Research in depression: endocrinology, epigenetics and neuroimaging) project we are examining possible epigenetic difference in some previously investigated target genes relevant to depression. To this end, methylation of the following genes were measured: NR3C1 (HPA axis), SLC6A4 (serotonin neurotransmitter function), and CD3ɛ (T cell receptor gene). We also looked at possible trans-generational transmission of epigenetic markers in a mother-baby sample.

Methods

DNA was isolated from depressed patients and controls and babies and a portion of the above genes, encompassing our regions of interest, were amplified by PCR. Percentage methylation levels were measured by pyrosequencing. mRNA was also measured for some gene products to see if function was related to methylation. HPA axis function was measured with serial saliva samples throughout the day.

Results

to date: Methylation was increased in the CD3ɛ promoter in depressed subjects relative to controls. In the total group, those exposed to ELA had significantly increased methylation at this site. Levels of CD3ɛ mRNA levels were inversely related to methylation. There were some relationships between maternal ELA and baby methylation at the sites examined.

Conclusions

Consistent with an allostatic model of ELA damage, our findings suggest an alteration in epigenetic function in acquired immunity and the HPA axis, mediated by ELA. Findings will be discussed.

Disclosure of interest

The authors have not supplied their declaration of competing interest.

Type
Symposium: How to Integrate Stress - (Epi) Genetics and Imaging and What Does It Tell Us
Copyright
Copyright © European Psychiatric Association 2017
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