European Psychiatry - Volume 41 - April 2017

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S18 25th European Congress of Psychiatry / European Psychiatry 41S (2017) S8–S52
Symposium: The role of the telomere-telomerase
system in psychiatric disorders and treatments:
Underlying mechanisms linking mental illness
with cellular aging
S034
Telomere length and depressive and
anxiety disorders: Longitudinal
associations and underlying
mechanisms
B. Penninx ∗, J. Verhoeven
VU University Medical Center, Psychiatry, Amsterdam, The
Netherlands
∗ Corresponding author.
Many psychiatric disorders have been associated with increased
risk of mortality and various aging-related somatic diseases. In
addition to unhealthy lifestyles, also various stress-related physio-
logical processes likely play a role in explaining these detrimental
health consequences of psychiatric disorders. The impact could be
visible at the cellular level, with psychiatric patients presenting
more signals of physiological aging for instance as determined by
measuring telomere length. In this talk we will first highlight the
current state-of-the art evidence that various psychiatric condi-
tions, including e.g. depression, anxiety and PTSD, are associated
with shorter telomere length. Second, we will provide results from
the Netherlands Study of depression and anxiety (n = 2981) that
tested longitudinal associations using 6 year data on psychiatric
status and telomere length. These results indicate that the asso-
ciation between depressive and anxiety disorders with telomere
length is stable over time, and doesn’t show many dynamic asso-
ciations. Finally, in the same study we have also tested to what
extent lifestyle and dysregulations of physiological stress systems
such as the immune, HPA-axis and autonomic nervous systems
are partly responsible for the observed shorter telomere length
in depressed or anxious patients. Results indicate that especially
smoking behavior and systemic inflammation partly contribute to
the shorter telomere length, but can’t completely explain found
associations.
In sum, this talk will highlight the current state-of-evidence for
an association between various psychiatric conditions with shorter
telomere length, and will provide insights into its dynamics and its
contributing mechanisms.
Disclosure of interest The authors have not supplied their decla-
ration of competing interest.
S035
The role of telomeres and telomerase
in the clinical effect and mechanism
of action of psychopharmacological
interventions
F.S. Bersani
Sapienza University of Rome, Department of Neurology and
Psychiatry, Roma, Italy
Originally studied in relation to aging and cancer research, telom-
eres and telomerase are now also investigated in relation to
psychiatric disorders and treatments. Based on findings emerg-
ing from clinical and preclinical data, we hypothesize that the
telomere–telomerase system represents a novel element medi-
ating the mechanism of action of certain psychopharmacological
interventions.
In this symposium I’ll present the preliminary evidence on the
complex translational relationships between specific psychiatric
medications (i.e. antidepressants, lithium and antipsychotics), the
telomere–telomerase system and clinical outcomes. The modula-
tion of intracellularWnt/b-catenin or PI3 K/Akt signaling pathways,
the interaction with BDNF and 5-HT, and the antioxidant proper-
ties could represent possible mechanisms by which the different
types of psychiatric medications could modulate telomere length
and telomerase activity. The potential of the telomere–telomerase
system in promoting cellular survival and/or function in the brain
and in the periphery could, in turn, represent a neurobiological sub-
strate through which these molecules can mediate the therapeutic
effect of such interventions.
Further, in the present symposium I’ll show data from our research
team on telomere length and telomerase activity in leukocytes pre-
dicting clinical response to serotonin–specific reuptake inhibitors
(SSRIs) in subjects with major depressive disorder.
Disclosure of interest The author has not supplied his declaration
of competing interest.
S036
Can reducing psychological distress
slow down the rate of telomere
attrition?
E. Epel ∗, J. Verhoeven
1 USA
2 VU university Amsterdam, VU university medical center,
Amsterdam, The Netherlands
∗ Corresponding author.
Specific types of cognitions and mental processes may lead to
greater stress arousal and may subsequently impact cell longevity.
The study of telomeres and telomere-related molecular sys-
tems may provide a pathway for exploring the link between
psychological domains and cell physiology. Based on findings
emerging from clinical and preclinical data, we hypothesize that
the telomere-telomerase systemcontributes to explain certain bio-
logical underpinnings of psychological interventions.
In this symposium we’ll present the preliminary evidence on
the complex translational relationships between specific psycho-
logical domains (i.e. childhood adversities, stressful life events,
mindfulness-based interventions and perceived distress), the
telomere-telomerase system and clinical outcomes. Further, we’ll
discuss preliminary data on the effect of mindfulness- and
meditation-based interventions on cellular ageing and disease-
associated molecular phenotypes.
Disclosure of interest The authors have not supplied their decla-
ration of competing interest.
S037
Evidence of accelerated biological
ageing in post-traumatic stress
disorder
D. Lindqvist
Lund, Sweden
Post-traumatic stress disorder (PTSD) is a common and debilitat-
ing condition, affecting between 10–20% of soldiers returning from
combat zones, and with even higher prevalence rates in Veterans
Affairs healthcare settings. PTSD is associatedwith an increased risk
for various medical illnesses, many of which are commonly seen
with older age. This raises the possibility that PTSD is associated
with accelerated biological aging at the cellular level. Accelerated
biological aging occurs when biological age outpaces chronolog-
ical age, and this process is driven by a number of biological
mechanisms including immune activation, oxidative stress, and
mitochondrial dysfunction.