European Psychiatry - Volume 41 - April 2017

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25th European Congress of Psychiatry / European Psychiatry 41S (2017) S8–S52 S19
In this workshop I will present data from our research group and
others pertaining to the biological mechanisms underlying acceler-
ated cellular aging in PTSD. Most, but not all, studies have found that
PTSD is associatedwith shortermean leukocyte telomere length, an
indicator of accelerated cellular aging. Mitochondrial dysfunction
has been implicated in PTSD and our research group found evidence
of a “u-shaped” relationship between PTSD symptom severity and
mitochondrial DNA copy number. For what concerns immunity,
we have recently found that PTSD subjects have increased blood
levels of pro-inflammatory markers, a more senescent and dys-
functional profile of NK cells and impaired synthesis of nitric oxide.
Finally, I will discuss the possibility of accelerated epigenetic aging
in combat-exposed individuals with and without PTSD, using DNA
methylation data.
Disclosure of interest The author has not supplied his declaration
of competing interest.
Symposium: How to Integrate Stress - (Epi)
Genetics and Imaging and What Does It Tell Us
S038
Stress Hormone System and
Epigenetics in Depression
V. O’Keane , C. Farrell , K. Doolin , J. Chai , N. O’leary ,
T. Frodl , L. Booji ∗, L. Tozzi
1 Psychiatry, Ireland
2 Trinity college institute of neurosciences, psychiatry, Dublin, Ireland
3 TCIN, psychiatry, Dublin, Ireland
4 TCIN, psychology, Dublin, Ireland
5 Magdeburg university, universitätsklinik für psychiatrie und
psychotherapie, Magdeburg, Ireland
6 Psychology, Montreal, Canada
∗ Corresponding author.
E-mail address: (L. Booji)
Background Exposure to early life adversity (ELA) has been iden-
tified 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 neurotransmit-
ter function), and CD3 (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 mea-
sured 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: Methylationwas increased in the CD3 promoter
in depressed subjects relative to controls. In the total group, those
exposed to ELA had significantly increased methylation at this site.
Levels of CD3 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 decla-
ration of competing interest.
S039
Stress and the serotonergic system,
observations from pet imaging
M. Spies∗ anzenberger
Medical university of Vienna, department of psychiatry and
psychotherapy, Vienna, Austria
∗ Corresponding author.
Introduction Stress response and the neuroendocrinologic fac-
tors through which it is mediated are disturbed in anxiety and
in affective disorders. While acute stress is thought to result in
hypothalamus-pituitary-adrenal- (HPA) axis hyperactivity (Vargh-
ese 2001), chronic stress may result in decreased HPA-response
(Booji 2013). Antidepressant treatment, on the other hand, is
thought to realign HPA–axis activity (Schüle 2007).
On the other hand, dysregulation within the serotonergic neuro-
transmitter system is understood as a central moderator in the
pathophysiology of affective and anxiety disorders. Serotonergic
transmission both regulates- and is regulated by- glucocorto-
coids. Cortisol results in an increase in serotonin synthesis and
releasewhile serotonergic transmission is thought to downregulate
HPA-axis activity (Lanfumey, 2008). Positron emission tomography
(PET) studies have demonstrated the link between the serotoner-
gic system and the HPA-axis in humans in vivo. For example, a
negative correlation between cortisol and 5HT1A receptor levels in
various brain regions has been shown (Lanzenberger, 2010). SERT
expression, on the other hand, was shown using PET to be positively
related to HPA-axis reactivity (Frokjaer 2013).
Methods n.a.
Aims Available literature on interactions between the HPA-axis
and the serotonergic system will be discussed with a focus on data
acquired via PET studies.
Results n.a.
Conclusions The interaction between the serotonergic system
and the HPA-axis is likely bilateral and may be understood as a
neurobiological link by which stress may foster the development
of depression and anxiety.
Disclosure of interest M. Spies has received travel grants from
AOP Orphan Pharmaceuticals AG, Janssen-Cilag Pharma Gmbh, and
Eli Lilly, workshop participation from Eli Lilly, and speaker hono-
raria from Janssen-Cilag Pharma Gmbh. R. Lanzenberger received
travel grants and conference speaker honoraria from AstraZeneca,
Lundbeck A/S, Roche Austria GmbH, Dr. Willmar Schwabe GmbH
& Co. KG, AOP Orphan Pharmaceuticals, and Janssen-Cilag Pharma
Gmbh.
S040
Association of stress hormone system,
epigenetics and imaging
T. Frodl ∗ ozzi arrel Doolin O’Keane
F. Pomares arballedo ooij
1 Otto-von-Guericke university Magdeburg, psychiatry and
psychotherapy, Magdeburg, Germany
2 Trinity college Dublin, psychiatry- Trinity college institute of
neuroscience, Dublin, Ireland
3 Trinity college Dublin, psychiatry-trinity college institute of
neuroscience, Dublin, Ireland
4 Queen’s university, psychology and psychiatry, Montreal, Canada
∗ Corresponding author.