Pharmacopsychiatry
DOI: 10.1055/s-0043-107033
Original Paper
© Georg Thieme Verlag KG Stuttgart · New York

Comparing the Immune-Genomic Effects of Vilazodone and Paroxetine in Late-Life Depression: A Pilot Study

Harris Eyre1, 2, 3, 4, Prabha Siddarth1, Natalie Cyr1, Hongyu Yang5, Steve Cole1, 6, Malcolm Forbes7, Helen Lavretsky1
  • 1Semel Institute for Neuroscience and Human Behavior, UCLA, Los Angeles, California, United State of America (USA)
  • 2Discipline of Psychiatry, University of Adelaide, Adelaide, South Australia, Australia
  • 3Department of Psychiatry, University of Melbourne, Melbourne, Victoria, Australia
  • 4IMPACT SRC, School of Medicine, Deakin University, Geelong, Victoria, Australia
  • 5Ahmanson-Lovelace Brain Mapping Center, Department of Neurology, UCLA, Los Angeles, California, USA
  • 6Department of Medicine, Hematology-Oncology, UCLA, Los Angeles, California, USA
  • 7School of Medicine, University of Queensland, Brisbane, Queensland, Australia
Further Information

Publication History

received 09 October 2016
revised 19 19 2017

accepted 21 March 2017

Publication Date:
25 April 2017 (eFirst)

Abstract

Background

Vilazodone is a novel antidepressant agent that combines selective serotonin (5-HT) reuptake inhibitor (SSRI) activity and 5-HT(1A) receptor partial agonist activity.

Objective

A pilot study was conducted to compare vilazodone (novel compound) and paroxetine (gold standard) on antidepressant effects, tolerability, and inflammation and immune modulation.

Methods

A 12-week, double-blind, randomized clinical trial was conducted with 56 nondemented older adults diagnosed with major depressive disorder (MDD). Between-group differences in mood, tolerability, and safety, as well as genomic markers of inflammation and immune modulation, were examined.

Results

Both treatment groups demonstrated similar improvement in depressed mood. Leukocyte gene expression profiles demonstrated reduction of specific proinflammatory gene transcripts and bioinformatic indications of reduced nuclear factor kappa B (NF-κB), activator protein (AP)-1, and cAMP response element binding (CREB) activity in the vilazodone group compared to the paroxetine group. Transcript origin analyses implicated monocytes and dendritic cells as the primary cellular origins of transcript reductions in the vilazodone-treated group.

Conclusions

Vilazodone’s antidepressant effects may be associated with reduction of proinflammatory gene expression and immune modulation. Further research is required.