The Neurobiology of Depressive Illness
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|ClinicalTrials.gov Identifier: NCT00168493|
Recruitment Status : Unknown
Verified May 2008 by Baker Heart Research Institute.
Recruitment status was: Recruiting
First Posted : September 15, 2005
Last Update Posted : May 20, 2008
We aim to determine why patients with depression are at an elevated risk for the development of coronary heart disease, and resolve whether the severity of a patient's depression has a counterpart in demonstrable abnormalities in brain chemistry. Studies will be completed in 28 patients with depression; both males and females. Patients will be studied both untreated and during administration of a selective serotonin re-uptake inhibitor (SSRI) antidepressant. They will be either newly diagnosed with depression, untreated patients suffering a recent relapse, or patients seeking to switch from a non-SSRI antidepressant due to non-response. The turnover of chemical messengers in the brain will be estimated by high internal jugular venous blood sampling and DNA will be isolated and examined from blood cells. Immune function will also be assessed. Whole body and cardiac sympathetic nervous activity will be determined, as well as microneurographic recording of muscle sympathetic nervous activity.
It is hypothesised that patients with depression and no existing demonstrable cardiac disease demonstrate:
Alterations in brain monoaminergic neurotransmitter turnover, resulting in sympathetic nervous activation and dysregulation of the baroreflex control to both the heart (vagal) and muscle vasoconstrictor sympathetic nerves; and Exhibit enhanced platelet reactivity predisposing them to thrombogenesis and myocardial ischaemia.
Therapeutic intervention with an SSRI will modify cardiac sympathetic function, baroreflex sensitivity or platelet reactivity in a fashion likely to reduce cardiac risk.
|Condition or disease||Intervention/treatment||Phase|
|Major Depression||Drug: antidepressants primarily selective serotonin reuptake inhibitors||Not Applicable|
|Study Type :||Interventional (Clinical Trial)|
|Estimated Enrollment :||40 participants|
|Intervention Model:||Single Group Assignment|
|Masking:||None (Open Label)|
|Official Title:||The Neurobiology of Depressive Illness: Causes and Consequences of Altered Brain Monoaminergic Function|
|Study Start Date :||June 2000|
|Estimated Primary Completion Date :||December 2008|
|Estimated Study Completion Date :||December 2009|
Active Comparator: intervention
there is no sham or placebo control arm It is a single arm study
Drug: antidepressants primarily selective serotonin reuptake inhibitors
normal clinical dosages used according to clinical response as determined by a psychiatrist
- level of sympathetic nervous system activity and its response to treatment [ Time Frame: 12 weeks ]
- clinical response to treatment [ Time Frame: 12 weeks ]
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT00168493
|Contact: David A Barton, MBBSFRANZCPfirstname.lastname@example.org|
|Contact: Murray Esler, PhD Fracp||61385321338||Murray.Esler@baker.edu.au|
|Baker Heart Research Institute||Recruiting|
|Melbourne, Victoria, Australia, 3|
|Contact: David A Barton, MBBS 61393428946 email@example.com|
|Principal Investigator: David a Barton, m|
|Principal Investigator:||Murray A Esler, MBBS Phd||Baker Heart Research Insitute|