European Psychiatry - Volume 33 - March 2016

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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.
EW276
RNA expression profiling in depressed
patients suggests retinoid-related
orphan receptor alpha as a biomarker
for antidepressant response
J. Hennings ∗ Uhr lengel eber ütz
C. Touma arina Ising olsboer ucae
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.
EW277
Markers of neurodegeneration in
patients with severe neuropsychiatric
disorders
T. Dokukina ∗ 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.
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.