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25th European Congress of Psychiatry / European Psychiatry 41S (2017) S8–S52


Disclosure of interest

The author has not supplied his declaration

of competing interest.


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


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


” 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



), Alpha-2-Macroglobulin (


) and Transforming Growth

Factor Beta 1 (


) 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


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


Disclosure of interest

The author has not supplied his declaration

of competing interest.


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



Intergenerational transmission of

well being–genetic and epigenetic


E. Unternaehrer

1 ,

, K. Greenlaw


, S. Hari Dass


, L.M. Chen



A.A. Bouvette-Turcot


, K. Cost


, K.J. O’Donnell


, H. Gaudreau



L. McEwen

4 , J. M


4 , M.

S. Kobor

4 , A.S

. Fleming

5 ,

L. Atkinson

6 , J.E.


7 , M.


8 , A.


2 ,

C.M.T. Greenwood

2 , M.

J. Meaney



McGill University, Douglas Mental Health University Institute,

Montreal, Canada


Lady Davis Institute, Centre for Clinical Epidemiology, Montreal,



Sick Kids, Department of Psychiatry, Toronto, Canada


University of British Columbia, Centre for Molecular Medicine and

Therapeutics, Vancouver, Canada


University of Toronto Mississauga, Department of Psychology,

Toronto, Canada


Ryerson University, Department of Psychology, Toronto, Canada


McGill University, Department of Psychology, Montreal, Canada


McMaster University, Department of Psychiatry & Behavioral

Neurosciences, Hamilton, Canada

Corresponding author.


Maternal mental well being influences offspring

development. Research suggests that an interplay between genetic

and environmental factors underlies this familial transmission of

mental disorders.


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.


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 (


= 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),