The Neurobiology of Depressive Illness

Major Depression Clinical Trial

Official title:

The Neurobiology of Depressive Illness: Causes and Consequences of Altered Brain Monoaminergic Function

Clinical Trial Details — Status: Recruiting

Administrative data

• NCT number: NCT00168493
• Other study ID #: NHMRC D-01
• Status: Recruiting
• Phase: N/A
• First received: September 10, 2005
• Last updated: May 19, 2008
• Start date: June 2000
• Est. completion date: December 2009

Study information

• Verified date: May 2008
• Source: Baker Heart Research Institute
• Contact: David A Barton, MBBSFRANZCP
• Phone: 61393428946
• Email: david.barton[@]bigpond.com
• Is FDA regulated: No
• Health authority: Australia: National Health and Medical Research Council
• Study type: Interventional

Clinical Trial Summary

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.

Recruitment information / eligibility

• Status: Recruiting
• Enrollment: 40
• Est. completion date: December 2009
• Est. primary completion date: December 2008
• Accepts healthy volunteers: No
• Gender: Female
• Age group: 18 Years to 75 Years

Eligibility

Inclusion Criteria:

• Major depression

Exclusion Criteria:

• heart disease diabetes hypertension psychosis significant suicidal risk dementia

Study Design

Allocation: Non-Randomized, Intervention Model: Single Group Assignment, Masking: Open Label, Primary Purpose: Treatment

Related Conditions & MeSH terms

• Depression
• Depressive Disorder
• Depressive Disorder, Major
• Major Depression

Intervention

Drug:
• antidepressants primarily selective serotonin reuptake inhibitors
normal clinical dosages used according to clinical response as determined by a psychiatrist

Locations

Country	Name	City	State
Australia	Baker Heart Research Institute	Melbourne	Victoria

Sponsors (2)

Lead Sponsor	Collaborator
Baker Heart Research Institute	National Health and Medical Research Council, Australia

Country where clinical trial is conducted

Australia, 

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	level of sympathetic nervous system activity and its response to treatment		12 weeks	No
Secondary	clinical response to treatment		12 weeks	No