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S210

24th European Congress of Psychiatry / European Psychiatry 33S (2016) S116–S348

synaptogenesis and stress response. MiRs are detectable in bio-

logical fluids; however, no data is available regarding the use of

plasma circulating miRs as markers of MDD, only whole blood or

serum being reported so far.

Objectives

We investigated plasma miR profiles as potential

markers for MDD in patients treated with antidepressants.

Aims

To detect and characterize differentially expressed miRs

in the plasma of MDD patients, before and after treatment with

escitalopram.

Methods

Bloodwas collected frompatients withMDD before and

after 12 weeks of treatment. Plasma profiles of 1008 miRs were

measured by real time PCR. The fold change of expression between

time points was calculated and a paired

t

test was used for sta-

tistical significance. Gene targets and pathways were assessed in

miRWalk2.0.

Results

From 222 plasma miRs expressed, 40 were significantly

different after treatment. Upregulated miRs (23) belonged to 43

pathways, down-regulated miRs (17) belonged to 46 pathways;

the top 5 significant pathways identified being pathways in cancer,

Wnt signalling, endocytosis, axon guidance and MAPK signalling.

Six of these miRs are common to all five pathways: miR-146a-5p,

miR-146b-5p, miR-221-3p, miR-24-3p, miR-26a-5p.

Conclusions

Our analysis of significant changes in plasma miRs

after escitalopram treatment of MDD might open new avenues for

the understanding of its mode of action and its side effects. To

our knowledge, this is the first study to assess miRs affected by

antidepressant treatment in plasma of MDD patients.

Disclosure of interest

The authors have not supplied their decla-

ration of competing interest.

http://dx.doi.org/10.1016/j.eurpsy.2016.01.393

EW276

RNA expression profiling in depressed

patients suggests retinoid-related

orphan receptor alpha as a biomarker

for antidepressant response

J. Hennings

1 ,

, M .

Uhr

2 , T. K

lengel

1 , P. W

eber

1 , B. P

ütz

1 ,

C. Touma

3 , C. D

arina

1 , M.

Ising

4 , F. H

olsboer

1 , S. L

ucae

4

1

Max Planck Institute of Psychiatry, Translational Psychiatry,

Munich, Germany

2

Max Planck Institute of Psychiatry, Core Unit Biobanking and

Molecular Biology, Munich, Germany

3

Max Planck Institute of Psychiatry, Department Stress Neurobiology

and Neurogenetics, Munich, Germany

4

Max Planck Institute of Psychiatry, Clinical Research, Munich,

Germany

Corresponding author.

Gene expression profiling may be a tool to identify markers of

antidepressant treatment response and new potential drug targets.

In a first step, we selected 12 males, age- and severity-matched

pairs of remitters and non-responders, and analyzed expression

profiles in peripheral blood at admission and after 2 and 5 weeks

of treatment using Illumina expression arrays. We identified 127

transcripts significantly associated with treatment response with

a minimal

P

-value of 9.41

×

10

4

(false discovery rate-corrected).

Analysis of selected transcripts in an independent replication sam-

ple of 142 depressed inpatients confirmed that lower expression of

retinoid-related orphan receptor alpha (RORa,

P

= 6.23

×

10

4

), ger-

minal center expressed transcript 2 (GCET2,

P

= 2.08

×

10

2

) and

chitinase 3-like protein 2 (CHI3L2,

P

= 4.45

×

10

2

) on admission

were associated with beneficial treatment response. In addition,

leukocyte-specific protein 1 (LSP1) significantly decreased after

5 weeks of treatment in responders (

P

= 2.91

×

10

2

). Additional

genetic, in vivo stress responsitivity data and murine hippocam-

pal gene expression findings corroborate our finding of RORa as

a transcriptional marker of antidepressant response. In summary,

using a genome-wide transcriptomics approach and subsequent

validation studies, we identified several transcripts including the

circadian gene transcript RORa that may serve as biomarkers indi-

cating antidepressant treatment response.

Disclosure of interest

The authors have not supplied their decla-

ration of competing interest.

http://dx.doi.org/10.1016/j.eurpsy.2016.01.394

EW277

Markers of neurodegeneration in

patients with severe neuropsychiatric

disorders

T. Dokukina

, M.

Makhrov , P. Korolevich , A. Pinchuk ,

A. Astashonok , T. Budko

Republican Scientific and Practical Centre for Mental Health,

Department of mental and behavioral disorders, Minsk, Belarus

Corresponding author.

The high frequency of occurrence and serious social consequences

of cognitive impairment allow us to consider them as an actual

general medical problem.

Objective

To describe the quantitative ratios of markers of

neurodegeneration (A 40, A 42, phosphorylated tau protein) in

patients with severe neuropsychiatric disorders.

Material and methods

The study included 82 patients with dif-

ferent cognitive impairment. Three groups: 35 patients with

schizophrenia, 26 patients with epilepsy and 21 patients with

autism. The results showed differences in the expression profile of

tau protein in patients with early and late onset of schizophrenia.

Variations of the quantitative ratio in plasma of amyloid peptide

A 40 were detected in the second experimental group (epilepsy).

A 40 concentrations were 13.8–38 pg/mL in the age group 28–39

years. At the same time, this protein was not detected in persons

older than 40 years. Amyloid A 42 was not detected in any of the

cases. Tau (concentration 30 pg/mL) is defined only in 1 patient.

Most of the persons with autismnoted the presence of twomarkers

simultaneously: tau protein (concentration 27.4 pg/mL) and amy-

loid A 40 (concentration 23–138 pg/mL).

Conclusion

It is shown that there is a high variability of the

proportion of the amyloid A 40 in patients with schizophrenia,

epilepsy and autism. Tau protein is detected only in the group

of patients with early-onset schizophrenia and in one case in a

patient with epilepsy. The results are important for the improve-

ment of diagnostic methods and development of etiopathogenic

therapy.

Disclosure of interest

The authors have not supplied their decla-

ration of competing interest.

http://dx.doi.org/10.1016/j.eurpsy.2016.01.395

EW278

Alterations of the

POMC-promoter-methylation and its

derivative alpha-MSH in a rodent

model for alcohol dependence

M. Muschler

, M. Rhein , H. Frieling , T. Hillemacher , S. Bleich

Medical School Hannover, Department of Psychiatry, Social

Psychiatry and Psychotherapy, Hannover, Germany

Corresponding author.

Introduction

Till this day the molecular mechanisms underlying

alcohol dependence are far from being understood in its entirety.

Repeatedly the HPA-axis got in the focus of research for alcohol

dependence. Many of these works show an association between

alcohol dependence and the answer of the HPA-axis on its different

levels. POMC and its derivative alpha-MSH as part of the HPA-

axis are supposed to mediate alcohol craving. To investigate the

role of alpha-MSH for craving we used a rodent model for alcohol

dependence.