Serotonin Transporter Genetic Variation and Amygdala Responses to Antidepressant Medications in Major Depression
Status:
Completed
Trial end date:
2012-04-01
Target enrollment:
Participant gender:
Summary
Major depressive disorder (MDD) is a highly prevalent, chronic and/or recurrent condition
with substantial morbidity and mortality. It is one of the leading causes of disability
worldwide. Despite significant advances in pharmacological treatment for depression over the
last two decades, a significant proportion of patients (10-20%) are resistant to currently
available treatment. The development of new effective treatment for depression is limited by
the fact that MDD is a heterogeneous disorder with subgroups based on variations in
etiological factors and treatment response. Functional magnetic resonance imaging (fMRI)
approaches offer promise in the prediction and evaluation of clinical response of
antidepressant treatment.
Previous fMRI studies have identified increased activity in dorso-lateral prefrontal cortex
(DLPFC) and decreased amygdala activity from the baseline as imaging markers of
antidepressant response in patients with MDD. However, these studies have examined MDD as a
homogenous group without specifying the type of patient group, and brain regions as a priori
hypothesis.We therefore need studies using combined genetics and neuroimaging measures as
biomarkers in the prediction and evaluation of clinical response to antidepressants. In this
study we attempted to determine imaging clinical efficacy markers in previously defined brain
regions (amygdala and prefrontal regions) for two classes of antidepressants (citalopram and
quetiapine extended release (XR)) with differential action on serotonin transporter
inhibition in a subgroup of MDD patients with high risk allele ( S/Lg) of serotonin
transporter gene polymorphism.