Ignite Creation Date:
2024-05-05 @ 11:53 AM
Last Modification Date:
2024-10-26 @ 9:15 AM
Study NCT ID:
NCT00168493
Status:
UNKNOWN
Last Update Posted:
2008-05-20
First Post:
2005-09-10
Brief Title:
The Neurobiology of Depressive Illness
Sponsor:
Baker Heart Research Institute
Organization:
Baker Heart Research Institute
Study Overview
Official Title:
The Neurobiology of Depressive Illness Causes and Consequences of Altered Brain Monoaminergic Function
Status:
UNKNOWN
Status Verified Date:
2008-05
Last Known Status:
RECRUITING
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
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 patients 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
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
Detailed Description:
None
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None