Desipramine for Improving Cellular Signaling and Decreasi... | NCT00320632

Studies
Desipramine for Improving Cellular Signaling and Decreasing Symptoms of Major Depression

NCT00320632

Sponsor

Harvard Medical School (HMS and HSDM)

Status

Completed

Last Update Posted

Aug 19, 2015Estimated

Enrollment

Phase

Phase 4

Conditions

Depression

Interventions

Desipramine

Countries

United States

Protocol Section

Identification Module Status Module Sponsor/Collaborators Module Oversight Module Description Module Conditions Module Design Module Arms/Interventions Module Outcomes Module Eligibility Module Contacts/Locations Module References Module IPD Sharing Statement Module

Results Section

Participant Flow Module Baseline Characteristics Module Outcome Measures Module Adverse Events Module More Info Module

Annotation Section

Annotation Module

Document Section

Large Document Module

Derived Section

Miscellaneous Info Module Condition Browse Module Intervention Browse Module

Protocol Section

Identification Module

NCT ID

Results Section

No data available

No data is available for this block.

Annotation Section

No data available

No data is available for this block.

Document Section

No data available

No data is available for this block.

Derived Section

Miscellaneous Info Module

Version Holder

ID	Type	Description	Link
R01MH015413	U.S. NIH Grant/Contract		View source

Status Module

Record Verification Date

Aug 2015

Overall Recruitment Status or Expanded Access Status

Completed

Last Known Status

Not provided

Delayed Posting

Not provided

Why Stopped

Not provided

Expanded Access Info

Start Date

Aug 1990

Primary Completion Date

Not provided

Completion Date

Jul 1993

First Submitted Date

Apr 28, 2006

First Submission Date that Met QC Criteria

Apr 28, 2006

First Posted Date

May 3, 2006Estimated

Results Waived

Not provided

Results First Submitted Date

Not provided

Results First Submitted that Met QC Criteria

Not provided

Results First Posted Date

Not provided

Certification/Extension (aka Delayed Results) First Submitted Date

Not provided

Certification/Extension First Submitted that Passed QC Review

Not provided

Certification/Extension First Posted Date

Not provided

Last Update Submitted Date

Aug 17, 2015

Last Update Posted Date

Aug 19, 2015Estimated

Sponsor/Collaborators Module

Responsible Party, by Official Title

JohnMooney, Principal Investigator, Harvard Medical School (HMS and HSDM)Principal Investigator

Lead Sponsor

Harvard Medical School (HMS and HSDM)OTHER

Collaborators

Name	Class
National Institute of Mental Health (NIMH)	NIH

Description Module

Brief Summary

This study will determine the effectiveness of desipramine in improving cellular signaling, and thereby decreasing symptoms of depression in people with major depressive disorder (MDD).

Detailed Description

MDD is a serious mental illness that can interfere with a person's ability to eat, sleep, work, and enjoy activities that were once pleasurable. It is characterized by several symptoms, including as the following: persistent sad, anxious, or "empty" mood; feelings of hopelessness or pessimism; and feelings of guilt, worthlessness, or helplessness. The receptor-G protein-adenylate cyclase enzyme complex (AC enzyme complex) is a major cell signaling system in the brain, blood, and other tissues in the body. Changes in this signaling system among blood cells have been observed in people with major depressive disorder. Research has shown that treatment with the benzodiazepine alprazolam corrects the signaling problem, and thereby improves symptoms of MDD. This study will determine whether impairments in the AC enzyme complex exist among depressed individuals. This study will also evaluate the effectiveness of desipramine, an antidepressant, in improving blood cell signaling, and thereby decreasing symptoms of depression in people with major depressive disorder.

Both healthy and depressed participants will be recruited for this study. All depressed participants in this study will first be assessed for depression severity using the Hamilton Depression Rating Scale. If eligible for the study, participants will be examined to determine AC enzyme complex functioning in both platelets and mononuclear leukocytes. A cohort of the depressed participants will be treated with desipramine. They will be examined to determine the drug's effect on AC enzyme complex functioning, as well as its effect on MDD symptoms, at Weeks 1, 4, and 6.

Design Module

Study Type

Interventional

Number of References to an Expanded Access Study

Not provided

Expanded Access Types

Not provided

Patient Registry

Not provided

Target Follow-Up Duration

Not provided

Phases

Phase 4

Interventional Study Design

Allocation

Biospecimen

No data available

No data is available for this block.

Enrollment

Name	Type	Description	Arm Group Labels	Other Names
Desipramine	Drug

Outcomes Module

Primary Outcomes

Measure	Description	Time Frame
Measured at Weeks 1, 4, and 6: Catecholamine metabolism and blood cell adenylate cyclase activity
Score on the 21-item Hamilton Depression Rating Scale

Secondary Outcomes

Not provided

Other Outcomes

Not provided

Eligibility Module

Eligibility Criteria

Inclusion Criteria:

Clinical diagnosis of MDD (as defined by SCID [DSM III-R] and a score of at least 15 on the 21-item Hamilton Depression Scale)
Able to swallow tablets, give urine and blood samples, and participate in periodic evaluations during the study
Healthy volunteers show no current Axis I or Axis II disorders and score less than 8 on the Hamilton Depression Scale

Exclusion Criteria:

Use of any of the following medications within the 2 weeks prior to study entry: psychoactive medication; aspirin; or nonsteroidal anti-inflammatory agents
Any alcohol or drug abuse within the 6 months prior to study entry
Any major medical disorder

Accepts Healthy Volunteers

Yes

Sex

All

Sex/Gender Based

Not provided

Sex/Gender Description

Not provided

Minimum Age

19 Years

Maximum Age

64 Years

Standard Ages

Adult

Study Population

Not provided

Sampling Method

Not provided

Contacts/Locations Module

Central Contacts

Not provided

Overall Officials

Name	Affiliation	Role
Joseph J. Schildkraut, MD	Department of Psychiatry, Harvard Medical School	Principal Investigator

Locations

Facility	Status	City	State	ZIP	Country	Contacts
Massachusetts Mental Health Center		Boston	Massachusetts	02115	United States

References Module

Citations

PubMed Identifier	Type	Citation	Retractions
2833319	Background	Mooney JJ, Schatzberg AF, Cole JO, Kizuka PP, Salomon M, Lerbinger J, Pappalardo KM, Gerson B, Schildkraut JJ. Rapid antidepressant response to alprazolam in depressed patients with high catecholamine output and heterologous desensitization of platelet adenylate cyclase. Biol Psychiatry. 1988 Mar 15;23(6):543-59. doi: 10.1016/0006-3223(88)90002-9.
9564442	Background	Mooney JJ, Samson JA, McHale NL, Colodzin R, Alpert J, Koutsos M, Schildkraut JJ. Signal transduction by platelet adenylate cyclase: alterations in depressed patients may reflect impairment in the coordinated integration of cellular signals (coincidence detection). Biol Psychiatry. 1998 Apr 15;43(8):574-83. doi: 10.1016/s0006-3223(97)00327-2.

ID	Term
D003863	Depression
D003865	Depressive Disorder, Major

ID	Term
D001526	Behavioral Symptoms
D001519	Behavior
D003866	Depressive Disorder
D019964	Mood Disorders

ID	Term
D003984	Dibenzazepines
D006575	Heterocyclic Compounds, 3-Ring
D000072471	Heterocyclic Compounds, Fused-Ring
D006571	Heterocyclic Compounds