Home
Search
Study Topics
Glossary
|
|
|
|
|
|
Sponsored by: |
Max-Planck-Institute of Psychiatry |
---|---|
Information provided by: | Max-Planck-Institute of Psychiatry |
ClinicalTrials.gov Identifier: | NCT00550485 |
The ABCB1-gene product P-glycoprotein is an integral membrane protein that actively transports substrates out of the intracellular compartment. One of the major sites of its action is the blood-brain-barrier. It is highly expressed in brain capillary endothelial cells and involved in limiting the access of substrates such as antidepressants to the CNS. A single nucleotide polymorphism (SNP) of the ABCB1-gene was recently identified showing a different treatment response to antidepressant drugs depending on the genotype. Therefore, it is assumed that healthy subjects with different genotypes of that SNP will be associated with significantly different brain levels of the antidepressant escitalopram after 6 days of intake. For determining intracerebral escitalopram levels, a 19-F magnetic resonance spectroscopy will be used. Sleep recordings are a useful bio-marker for effects of antidepressants on the CNS. Selective 5-HT1-reuptake inhibitors (e.g. escitalopram) cause a suppression of REM sleep and a stronger fragmentation of sleep compared to untreated subjects. Higher plasma levels of antidepressants affected the sleep to a greater extent than lower levels. In line with this finding, we suppose that sleep EEG recordings of healthy subjects with different genotypes of the above mentioned SNP will be differently affected after taking 6 days escitalopram. In addition, there is good evidence that sleep is involved in various forms of memory processing. For example, it has been repeatedly shown that the performance in motor tasks (procedural learning) is correlated with the amount of stage 2 NonREM and REM sleep, respectively. Hence we hypothesize, that a drug-induced impairment of sleep (e. g. reduction of REM sleep) is associated with an impairment of procedural learning. In addition, effects of drug intake on the gene expression in lymphocytes and metabolic changes will be assessed. Functional magnetic resonance imaging will be applied to detect potential drug-induced changes of corticolimbic circuitries.
Condition | Intervention |
---|---|
Pharmacokinetics |
Drug: escitalopram |
Study Type: | Interventional |
Study Design: | Basic Science, Open Label, Parallel Assignment |
Official Title: | Blood-Brain-Barrier Permeability of Escitalopram Depending on Genetic Polymorphisms of the ABCB1-Gene: Effect on Sleep and Procedural Learning |
Estimated Enrollment: | 300 |
Study Start Date: | October 2007 |
Estimated Study Completion Date: | June 2009 |
Estimated Primary Completion Date: | March 2009 (Final data collection date for primary outcome measure) |
Arms | Assigned Interventions |
---|---|
1
Healthy subjects with a single nucleotide polymorphism (SNP) of the ABCB1-gene (Genotype A)
|
Drug: escitalopram
escitalopram 10 mg
|
2
Healthy subjects with a single nucleotide polymorphism (SNP) of the ABCB1-gene (Genotype B)
|
Drug: escitalopram
escitalopram 10 mg
|
Ages Eligible for Study: | 20 Years to 60 Years |
Genders Eligible for Study: | Male |
Accepts Healthy Volunteers: | Yes |
Inclusion Criteria:
Exclusion Criteria:
Contact: Axel Steiger, MD | 0049 8930622 ext 236 | steiger@mpipsykl.mpg.de |
Contact: Michael Kluge, MD | 0049 8930622 ext 396 | kluge@mpipsykl.mpg.de |
Germany | |
Max Planck Institute of Psychiatry | Recruiting |
Munich, Germany, 81667 | |
Contact: Axel Steiger, MD 0049 8930622 ext 236 steiger@mpipsykl.mpg.de | |
Contact: Michael Kluge, MD 0049 8930622 ext 396 kluge@mpipsykl.mpg.de |
Principal Investigator: | Axel Steiger, MD | Max-Planck-Institute of Psychiatry |
Responsible Party: | Max-Planck-Institute of Psychiatry ( Axel Steiger, MD ) |
Study ID Numbers: | L3/2005 |
Study First Received: | October 29, 2007 |
Last Updated: | April 21, 2008 |
ClinicalTrials.gov Identifier: | NCT00550485 |
Health Authority: | Germany: Federal Institute for Drugs and Medical Devices |
Dexetimide Citalopram Serotonin |
Parasympatholytics Neurotransmitter Uptake Inhibitors Neurotransmitter Agents Molecular Mechanisms of Pharmacological Action Cholinergic Antagonists Anti-Dyskinesia Agents Physiological Effects of Drugs Psychotropic Drugs Antiparkinson Agents Cholinergic Agents |
Serotonin Uptake Inhibitors Pharmacologic Actions Muscarinic Antagonists Serotonin Agents Autonomic Agents Therapeutic Uses Peripheral Nervous System Agents Antidepressive Agents, Second-Generation Central Nervous System Agents Antidepressive Agents |