Desipramine for Improving Cellular Signaling and Decreasing Symptoms of Major Depression

NCT00320632 | Completed Phase 4

• 1 other identifier: R01MH015413
• Study Type: interventional
• Target: 43
• Locations: 1 country
• Sites: 1

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).

Conditions

Depression

Keywords

Major Depressive Disorder; MDD

Outcome Measures

Primary Outcomes (2)

• Measured at Weeks 1, 4, and 6: Catecholamine metabolism and blood cell adenylate cyclase activity

• Score on the 21-item Hamilton Depression Rating Scale

Interventions

Desipramine DRUG

Eligibility Criteria

• Age: 19 Years - 64 Years
• Sex: all
• Healthy Volunteers: Yes
• Age Groups: Adult (18-64)

You may qualify if:

• 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

You may not qualify if:

• 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

Sponsors & Collaborators

• Harvard Medical School (HMS and HSDM): lead
• National Institute of Mental Health (NIMH): collaborator

Study Sites (1)

Massachusetts Mental Health Center

Boston, Massachusetts, 02115, United States

Location

Related Publications (3)

• 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.

  PMID: 2833319 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.

  PMID: 9564442 BACKGROUND

• Mooney JJ, Samson JA, Hennen J, Pappalardo K, McHale N, Alpert J, Koutsos M, Schildkraut JJ. Enhanced norepinephrine output during long-term desipramine treatment: a possible role for the extraneuronal monoamine transporter (SLC22A3). J Psychiatr Res. 2008 Jul;42(8):605-11. doi: 10.1016/j.jpsychires.2007.07.009. Epub 2007 Aug 28.

  PMID: 17727882 DERIVED

MeSH Terms

Conditions

Depression; Depressive Disorder, Major

Interventions

Desipramine

Condition Hierarchy (Ancestors)

Behavioral Symptoms; Behavior; Depressive Disorder; Mood Disorders; Mental Disorders

Intervention Hierarchy (Ancestors)

Dibenzazepines; Heterocyclic Compounds, 3-Ring; Heterocyclic Compounds, Fused-Ring; Heterocyclic Compounds

Study Officials

• Joseph J. Schildkraut, MD

  Department of Psychiatry, Harvard Medical School

  PRINCIPAL INVESTIGATOR

Study Design

• Study Type: interventional
• Phase: phase 4
• Allocation: NON RANDOMIZED
• Masking: NONE
• Purpose: TREATMENT
• Intervention Model: SINGLE GROUP
• Sponsor Type: OTHER
• Responsible Party: PRINCIPAL INVESTIGATOR
• PI Title: Principal Investigator

Study Record Dates

• First Submitted: April 28, 2006
• First Posted: May 3, 2006
• Study Start: August 1, 1990
• Study Completion: July 1, 1993
• Last Updated: August 19, 2015

Record last verified: 2015-08

Locations

US (1)