European Psychiatry - Volume 41 - April 2017

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25th European Congress of Psychiatry / European Psychiatry 41S (2017) S69–S105 S103
Conclusions Our preliminary findings suggest that ACCN1 (ASIC2)
gene could be involved in modulating the susceptibility of BD
patients to develop renal dysfunctions induced by chronic Li treat-
ment.
Disclosure of interest The authors have not supplied their decla-
ration of competing interest.
O096
Association between two
single-nucleotide polymorphism of
TAAR1 gene and suicide attempts
A. Zdanowicz ∗, A. Sakowicz , E. Kusidel , P. Wierzbinski
1 Medical University, Department of Adult Psychiatry, Lodz, Poland
2 Medical University, Department of Medical Biotechnology, Lodz,
Poland
3 University of Lodz, Department of Spatial Econometrics, Lodz,
Poland
4 Medsolver- Psychological and Psychiatric Clinic, Lodz, Poland
∗ Corresponding author.
Introduction TAAR1 is a G protein-coupled receptor expressed
broadly throughout the brain. Recently, TAAR1 has been demon-
strated to be an important modulator of the dopaminergic,
serotonergic and glutamatergic activity.
Aims Assessment of the relation between two single-nucleotide
polymorphisms of TAAR1 gene, suicide attempts and alcohol abuse.
Methods A total of 150 Polish patients were included, 59 sub-
jects after suicide attempt vs. 91 controls. The chosen SNPs
(rs759733834 and rs9402439) were studied using RFLP-PCR meth-
ods. The Hardy-Weinberg equilibrium was tested in control group.
Statistical tests Chi2 or Yeates Chi2 Test were used.
Results The mean age of study subjects and controls was:
38 ± 12.3 and 42 ±12.8 respectively; 49% study males vs. 54% male
controls. We did not observe the association between the carriage
of the genotypes GG, GA and AA of rs759733834 polymorphisms
in either of the groups. The distribution of genotypes in respect
to rs9402439 polymorphism (CC, CG, GG) was also insignificant.
Among patients with alcohol dependence, the frequency G allele
of rs9402439 polymorphismwas lower compared to non-addicted
ones (27 vs. 47%) P < 0.01.
Conclusions TAAR1 polymorphisms rs759733834 and rs9402439
are not related to suicide attempts. The carriage of allele G of
rs9402439 polymorphism is related to lower risk of alcohol addic-
tion OR 0.40 95%Cl 0.20–0.81. To our knowledge, this is the first
study on the TAAR1 receptor and the risk of suicide and it might
offer a new insight into genetic etiology of TAAR1 receptor.
Disclosure of interest The authors have not supplied their decla-
ration of competing interest.
O097
Verbal learning and memory in at-risk
mental state and first episode
psychosis patients and their correlates
to brain structural alterations
L. Egloff ∗ enz , E. Studerus , U. Heitz , S. Menghini-Müller ,
F. Harrisberger , S. Ittig , K. Beck , L. Leanza , C. Andreou ,
A. Riecher-Rössler , S. Borgwardt
University of Basel Psychiatric Hospital, Department of Psychiatry,
Basel, Switzerland
∗ Corresponding author.
Introduction Patients with a first episode psychosis (FEP) have
repeatedly been shown to have gray matter (GM) volume alter-
ations. Some of these neuroanatomical abnormalities are already
evident in the at-risk mental state (ARMS) for psychosis. Not only
GM alterations but also neurocognitive impairments predate the
onset of frank psychosis with verbal learning and memory (VLM)
being among themost impaireddomains. Yet, their interconnection
with alterations in GM volumes remains ambiguous.
Objective To evaluate associations of different subcortical GM
volumes in the medial temporal lobe with VLM performance in
ARMS and FEP patients.
Methods Data were collected within the prospective Früherken-
nung von Psychosen (FePsy) study, which aims to improve the early
detection of psychosis. VLM was assessed using the California Ver-
bal Learning Test (CVLT) and its latent variables Attention Span
(AS), Learning Efficiency (LE), Delayed Memory (DM) and Inaccu-
rate Memory (IM). Structural images were acquired using a 3 Tesla
magnetic resonance imaging scanner.
Results Data from 59 ARMS and 47 FEP patients were ana-
lysed. Structural equation models revealed significant associations
between the amygdala and AS, LE and IM; thalamus and LE and IM;
and the caudate, hippocampus and putamen with IM. However,
none of these significant results withstood correction for multiple
testing.
Conclusions Although VLM is among themost impaired cognitive
domains in emerging psychosis, we could not find an association
between lowperformance in this domain and reductions in subcor-
tical GM volumes. Our results suggest that deficits in this domain
may not stem from alterations in subcortical structures.
Disclosure of interest The authors have not supplied their decla-
ration of competing interest.
O098
The effects of deep-brain magnetic
stimulation (DMS) on white matter
deficits: New mechanism in major
depressive disorder (MDD) treatment
Y. Zhang Zhang eng Guo Zhang owen
X.M. Li ∗
1 University of Saskatchewan, Department of Psychiatry, Saskatoon,
Canada
2 University of Alberta, Department of Psychiatry, Edmonton, Canada
3 Fourth Military Medical University, Department of Psychiatry,
Xi’An, China
4 Xinxiang Medical University, Department of Psychology, Xinxiang,
China
∗ Corresponding author.
Deep-brain magnetic stimulation (DMS) is an effective therapy
for various neuropsychiatric disorders including major depression
disorder. The molecular and cellular mechanisms underlying the
impacts of DMS on the brain remain unclear. Studies have reported
abnormalities in the white matter of depressive brains, suggest-
ing the involvement of myelin and oligodendrocyte pathologies
in the development of major depressive disorder. In this study,
we use a cuprizone induced demyelination animal model to
generate depressive like behaviours and white matter and oligo-
dendrocyte damages. Meanwhile, we treated the animal with
DMS 20minutes daily during the cuprizone challenge or recovery
period. Behavioural tests, including nesting, new objective recog-
nition, working memory and depression-like behaviours were
tested periodically. Histological staining and western blotting were
used to examine the underlying mechanism of DMS. We found
that DMS reverse cuprizone induced behavioural deficits in acute
demyelination but not during the recovery period. DMS alleviated
demyelination and inflammation induced by cuprizone. During the
recovery period, DMS had no impacts on overall neural progenitor
cell proliferation, but enhanced the maturation of oligodendrocyte.
This data suggest that DMS may be a promising treatment option
for improving white matter function in psychiatric disorders and
neurological diseases in future.