The Neurobiology of Depressive Illness

The recruitment status of this study is unknown because the information has not been verified recently.
Verified May 2008 by Baker Heart Research Institute.
Recruitment status was  Recruiting
Sponsor:
Collaborator:
National Health and Medical Research Council, Australia
Information provided by:
Baker Heart Research Institute
ClinicalTrials.gov Identifier:
NCT00168493
First received: September 10, 2005
Last updated: May 19, 2008
Last verified: May 2008

September 10, 2005
May 19, 2008
June 2000
December 2008   (final data collection date for primary outcome measure)
level of sympathetic nervous system activity and its response to treatment [ Time Frame: 12 weeks ] [ Designated as safety issue: No ]
Not Provided
Complete list of historical versions of study NCT00168493 on ClinicalTrials.gov Archive Site
clinical response to treatment [ Time Frame: 12 weeks ] [ Designated as safety issue: No ]
Not Provided
Not Provided
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The Neurobiology of Depressive Illness
The Neurobiology of Depressive Illness: Causes and Consequences of Altered Brain Monoaminergic Function

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.

Not Provided
Interventional
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Allocation: Non-Randomized
Intervention Model: Single Group Assignment
Masking: Open Label
Primary Purpose: Treatment
Major Depression
Drug: antidepressants primarily selective serotonin reuptake inhibitors
normal clinical dosages used according to clinical response as determined by a psychiatrist
Active Comparator: intervention
there is no sham or placebo control arm It is a single arm study
Intervention: Drug: antidepressants primarily selective serotonin reuptake inhibitors
Not Provided

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Recruiting
40
December 2009
December 2008   (final data collection date for primary outcome measure)

Inclusion Criteria:

  • Major depression

Exclusion Criteria:

  • heart disease diabetes hypertension psychosis significant suicidal risk dementia
Female
18 Years to 75 Years
No
Contact: David A Barton, MBBSFRANZCP 61393428946 david.barton@bigpond.com
Contact: Murray Esler, PhD Fracp 61385321338 Murray.Esler@baker.edu.au
Australia
 
NCT00168493
NHMRC D-01
No
Dr David Barton, Baker Heart Research Institute
Baker Heart Research Institute
National Health and Medical Research Council, Australia
Principal Investigator: Murray A Esler, MBBS Phd Baker Heart Research Insitute
Baker Heart Research Institute
May 2008

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP