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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


Telomere length and depressive and

anxiety disorders: Longitudinal

associations and underlying


B. Penninx

, J. Verhoeven

VU University Medical Center, Psychiatry, Amsterdam, The


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 (


= 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


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.


The role of telomeres and telomerase

in the clinical effect and mechanism

of action of psychopharmacological


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


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.


Can reducing psychological distress

slow down the rate of telomere


E. Epel

1 ,

, J. Verhoeven





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.


Evidence of accelerated biological

ageing in post-traumatic stress


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.