SYMPOSIA

Abstracts of the Invited Speakers
[PS-19]
Symposium Title: Are the effects of psychopharmacological and other therapeutic approaches neuroregenerative or
neurodegenerative? Review of recent data
Is the effect of psychotropic drugs neurodegenerative or neuroprotective?
Ömer Aydemir
Department of Psychiatry, Celal Bayar University, Manisa, Turkey
E-mail: soaydemir@hotmail.com
Various stress experiences affect gene expression of neurotrophic/growth factors in the hippocampus. Among the neurotrophic factors,
brain-derived neurotrophic factor (BDNF) has the most prominent role. With the stress producing effects of early life traumas, the level
of BDNF decreases and susceptibility to depression develops. Recurrent and insufficiently treated depressive episodes have further
impact on decreased BDNF and increase neuronal atrophy. Decreased level of BDNF in patients with major depressive disorder has been
demonstrated in many studies and BDNF levels increase after antidepressant treatment, along with symptom recovery, in comparison
to those seen in healthy control subjects. This increase cannot be achieved in patients that do not respond to antidepressant treatment.
The neuroprotective effect of antidepressants are mediated by mitogen activated protein kinases/extracellular regulated kinases (MAPK/
ERK) and wingless/glycogen synthase kinases (Wnt/GSK). In a meta-analysis, 23 studies were evaluated and data for 1504 patients were
subjected to statistical analysis. The effect size was calculated as 0.62 (95% confidence interval: 0.36-0.88). As a result of meta-regression,
the change in the level of serum BDNF after antidepressant treatment was independent of the change in depressive symptomatology,
duration of treatment, and history of antidepressant use. As clinical improvement obtained with antidepressant treatment persists, the
level of serum BDNF remains unchanged.
Beside antidepressants, mood stabilizers, especially lithium have been studied with respect to neuroplasticity. Neuroprotective effects of
mood stabilizers are mediated by increasing transcriptional activity of (cAMP response element binding protein) CREB, inhibiting GSK-3B
and increasing the expression of BDNF. In studies both with lithium and valproate, increased cerebral grey matter volume was reported.
In lithium studies increases in left anterior cingulate volume, right anterior cingulate volume, hippocampal volume and amygdala volume,
and in valproate studies an increase in left anterior cingulate volume were found. Both mood stabilizers are associated with increased
hippocampal N-acetyl aspartate level.
Antipsychotic drugs do not have a group effect. While haloperidol does not have any effect on phosphorilated ERK (pERK), olanzapine
increases it. Haloperidol also decreases the level of BDNF and is suggested to have neurotoxic effects. Among the other antipsychotics,
clozapine, quetiapine and risperidone prevent cell death. It has been demonstrated that clozapine and quetiapine increase the level of
BDNF. Quetiapine is suggested to increase proliferation of mature neurons, although there is no evidence that clozapine and olanzapine
have the same effect.
Key words: Psychotropic drugs, neuroplasticity, neurodegeneration, neuroprotective effect
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S90
Effect of psychotherapy on neurogenesis
Mine Özmen
Istanbul Universit Cerrahpasa Medical Faculty, Department of Psychiatry, İstanbul, Turkey
E-mail: drmineozmen@yahoo.com
Adverse life experiences in childhood are considered to be associated with emotional and cognitive development as well as brain
structure and functions. It is suggested that they might reduce neurogenesis, which in turn may cause memory, learning, functional
stress response disturbances. It is known that hippocampal neurogenesis is affected by stress, hormones, aging, environment and activity.
Exposure to acute or chronic stress may result in suppression of one or more phases of neurogenesis. In animal studies, reduction of
neurogenesis in the caudal part of the hippocampus was shown after maternal separation of 3-weeks old rats. Although it was reported
that the suppression was reversible after appropriate time and treatment in some studies, some other writers suggest that early life stress
in the first 2 weeks can cause irreversible reduction in neurogenesis. Besides, there is an argument that neurogenesis can not increase by
learning in the animals which were exposed to prenatal stress. One suggested reason for this lifetime persistency of reduced neurogenesis
is that stress occurring in early childhood coincides with the development of dentate gyrus. It has been shown that corticosteroids
S90 Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org