The Neurobiology of Depressive Illness

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

Sponsors

Lead Sponsor: Baker Heart Research Institute

Collaborator: National Health and Medical Research Council, Australia

Source Baker Heart Research Institute
Brief 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.

Overall Status Unknown status
Start Date June 2000
Completion Date December 2009
Primary Completion Date December 2008
Phase N/A
Study Type Interventional
Primary Outcome
Measure Time Frame
level of sympathetic nervous system activity and its response to treatment 12 weeks
Secondary Outcome
Measure Time Frame
clinical response to treatment 12 weeks
Enrollment 40
Condition
Intervention

Intervention Type: Drug

Intervention Name: antidepressants primarily selective serotonin reuptake inhibitors

Description: normal clinical dosages used according to clinical response as determined by a psychiatrist

Arm Group Label: intervention

Eligibility

Criteria:

Inclusion Criteria:

- Major depression

Exclusion Criteria:

- heart disease diabetes hypertension psychosis significant suicidal risk dementia

Gender: Female

Minimum Age: 18 Years

Maximum Age: 75 Years

Healthy Volunteers: No

Overall Official
Last Name Role Affiliation
Murray A Esler, MBBS Phd Principal Investigator Baker Heart Research Insitute
Overall Contact

Last Name: David A Barton, MBBSFRANZCP

Phone: 61393428946

Email: [email protected]

Location
Facility: Status: Contact: Investigator: Baker Heart Research Institute David A Barton, MBBS 61393428946 [email protected] David a Barton, m Principal Investigator
Location Countries

Australia

Verification Date

May 2008

Responsible Party

Name Title: Dr David Barton

Organization: Baker Heart Research Institute

Keywords
Has Expanded Access No
Condition Browse
Number Of Arms 1
Arm Group

Label: intervention

Type: Active Comparator

Description: there is no sham or placebo control arm It is a single arm study

Study Design Info

Allocation: Non-Randomized

Intervention Model: Single Group Assignment

Primary Purpose: Treatment

Masking: None (Open Label)

Source: ClinicalTrials.gov