Cognitive deficits in major depression seem explicable by the well-recognized concept of impaired neuroplasticity in mood disorders. This concept initially emerged from preclinical evidence that antidepressants phosphorylate and therefore activate the cyclic AMP response element binding protein (CREB) that is essential for synaptic plasticity. Nevertheless, the question remains whether the activation of CREB by antidepressants is relevant for the remission of cognitive deficits in patients. We addressed this issue by investigating the cognitive improvement during treatment with either citalopram or reboxetine because these antidepressants are different in their capacity to increase phosphorylated CREB (pCREB). Besides the pharmacological treatment groups, another group of patients was treated exclusively with psychotherapy.
We randomly assigned forty-five depressive patients to one of three treatment groups (Citalopram, Reboxetin or interpersonal psychotherapy (IPT)). At baseline, day 7 and day 28 we assessed the severity of depression and the cognitive performance with respect to cognitive flexibility, memory and attention. We measured pCREB with an enzyme linked immuno sorbent assay (ELISA).
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
BASIC_SCIENCE
Masking
NONE
Enrollment
45
20 to 30 mg per day for 4 weeks
4 to 8 mg per day for 4 weeks
Zentrum für Integrative Psychiatrie
Kiel, Germany
cognitive performance with respect to cognitive flexibility, memory and attention
Time frame: 4 weeks
CREB-phosphorylation in T-Lymphocytes
Time frame: 4 weeks
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