European Psychiatry - Volume 41 - April 2017

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25th European Congress of Psychiatry / European Psychiatry 41S (2017) S8–S52 S29
Disclosure of interest The author has not supplied his declaration
of competing interest.
S070
Identification of a long lasting stress
signatures associated with enhanced
vulnerability for depression by using
‘omics and cross species approaches
A. Cattaneo
King’s college London, psychological medicine, London, United
Kingdom
Depression results from the interplay of vulnerability genes
with environmental factors, a phenomenon named as ‘gene-
environment (GxE) interaction’. To date, GxE interaction studies
have been limited to hypothesis-based candidate genes, since
genome-wide (GWAS)-based GxE interaction studies would
require enormous datasets with genetics, environmental and clin-
ical variables. We used a novel, cross-species and cross-tissues
“omics” approaches to identify genes predicting depression in
response to stress in GxE interactions. We integrated the transcrip-
tome and miRNome profiles from the hippocampus of adult rats
exposed to prenatal stress (PNS) with transcriptome data obtained
from blood mRNA of adult humans exposed to early life trauma,
using a stringent statistical analyses pathway. Network analysis of
the integrated gene lists identified the Forkhead box protein O1
(FOXO1), Alpha-2-Macroglobulin (A2M) and Transforming Growth
Factor Beta 1 (TGFB1) as candidates to be tested for GxE interactions,
in two GWAS samples of adults either with a range of childhood
traumatic experiences (Grady Study Project, Atlanta, USA) or with
childhood emotional abuse only (Helsinki Birth Cohort Study, Fin-
land). Six FOXO1 SNPs showed significant GxE interactions with
emotional abuse in the Grady Study that survived stringent per-
mutation analyses and were all replicated in the Helsinki study.
In addition, other SNPs in all the three genes showed significant
GxE interactions with emotional, physical and sexual abuse in
the Grady Study. We therefore provide a successful ‘hypothesis-
free’ approach for the identification and prioritization of candidate
genes for GxE interaction studies that can be investigated in GWAS
datasets.
Disclosure of interest The author has not supplied his declaration
of competing interest.
S071
Epigenetic signatures of early life
adversities in animal models: A role
for psychopathology vulnerability
M.A. Riva
University of Milan, Department of Pharmacological and
Biomolecular Sciences, Milan, Italy
Stressful experiences early in life (ELS) represent one of the most
relevant factors for the vulnerability to psychopathologies. Epige-
netic changes, such as DNA methylation, have emerged as a major
mechanism through which ELS can alter adult behaviour leading to
persistent changes of gene regulation.
We performed DNA methylation analyses in the hippocampus and
prefrontal cortex of adult rats exposed to stress during gestation
(PNS), a model that is associated with persistent behavioral alter-
ations relevant for psychiatric disorders.
Using an epigenome-wide analysis, an overlap of 893 differentially
methylated genes was observed between hippocampus and pre-
frontal cortex of adult male and female rats exposed to PNS. The
list includes several genes previously associated with schizophre-
nia and other psychiatric conditions, such as calciumand potassium
voltage operated channels as well as GABA and glutamate receptor
subunits. By restricting the overlap to genes that were modulated
in the same direction, we identified miR-30a as being less methyl-
ated in PNS rats. Interestingly one of the targets for this miRNA is
the neurotrophin BDNF, whose expression was indeed reduced as
a consequence of the prenatal manipulation. Interestingly chronic
treatment of PNS rats with the multi-receptor modulator lurasi-
done during adolescencewas able to prevent the changes inmiR30a
and BDNF expression.
These results highlight the importance for the identification of
methylation signatures through which stress exposure early in
life could engrave on the outcome of the adult phenotype, and
may allow the identification of novel genes and pathways that are
affected as a consequence of ELS.
Disclosure of interest M.A.R. has received compensation as
speaker/consultant from Lundbeck, Otzuka, Sumitomo Dainippon
Pharma and Sunovion. He has received research grants from Lund-
beck, Sumitomo Dainippon Pharma and Sunovion.
Symposium: Intergenerational transmission of
parenting: Epigenetic, genetic, and psychological
mechanisms
S072
Intergenerational transmission of
well being–genetic and epigenetic
mechanisms
E. Unternaehrer ∗, K. Greenlaw , S. Hari Dass , L.M. Chen ,
A.A. Bouvette-Turcot , K. Cost , K.J. O’Donnell , H. Gaudreau ,
L. McEwen acIsaac S. Kobor . Fleming
L. Atkinson Lydon Steiner Ciampi
C.M.T. Greenwood J. Meaney
1 McGill University, Douglas Mental Health University Institute,
Montreal, Canada
2 Lady Davis Institute, Centre for Clinical Epidemiology, Montreal,
Canada
3 Sick Kids, Department of Psychiatry, Toronto, Canada
4 University of British Columbia, Centre for Molecular Medicine and
Therapeutics, Vancouver, Canada
5 University of Toronto Mississauga, Department of Psychology,
Toronto, Canada
6 Ryerson University, Department of Psychology, Toronto, Canada
7 McGill University, Department of Psychology, Montreal, Canada
8 McMaster University, Department of Psychiatry & Behavioral
Neurosciences, Hamilton, Canada
∗ Corresponding author.
Introduction Maternal mental well being influences offspring
development. Research suggests that an interplay between genetic
and environmental factors underlies this familial transmission of
mental disorders.
Objectives To explore an interaction between genetic and envi-
ronmental factors to predict trajectories of maternal mental well
being, and to examine whether these trajectories are associated
with epigenetic modifications in mothers and their offspring.
Method We assessed maternal childhood trauma and rearing
experiences, prenatal and postnatal symptoms of depression and
stress experience from6 to 72months postpartum, and genetic and
epigenetic variation in a longitudinal birth-cohort study (n = 262)
(Maternal adversity, vulnerability and neurodevelopment project).
We used latent class modeling to describe trajectories in maternal
depressive symptoms, parenting stress, marital stress and general
stress, taking polygenetic risk for major depressive disorder (MDD),