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Toward an anti-inflammatory strategy for depression.

¹Department of Neuroscience, Carleton University Ottawa, ON, Canada.

Frontiers in Behavioral Neuroscience

|May 12, 2011

Summary

Depression involves immune system changes, including elevated pro-inflammatory cytokines and altered immune cell trafficking. Anti-inflammatory treatments may offer therapeutic benefits alongside traditional antidepressants.

Keywords:

anhedonia cytokine depression inflammatory neurogenesis

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Area of Science:

Neuroimmunology
Psychiatry

Background:

Clinical depression is linked to immune system alterations.
Studies show changes in adaptive immune cell trafficking and elevated innate immune messengers in depressed patients.
Animal models implicate cytokines like interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α in depression.

Purpose of the Study:

To review evidence for pro-inflammatory cytokine involvement in depression.
To explore the potential of anti-inflammatory agents and trophic cytokines as antidepressant therapies.

Main Methods:

Review of existing human patient studies and stressor-based animal models.
Analysis of immune system indicators, including cytokines and C-reactive protein.
Examination of immune cell populations, such as T lymphocytes.

Main Results:

Depression is associated with immune dysregulation, including elevated pro-inflammatory cytokines and altered immune cell distribution.
Specific inflammatory markers and reduced T lymphocytes may serve as depression biomarkers.
Emerging evidence suggests anti-inflammatory agents could complement conventional antidepressant treatments.

Conclusions:

Pro-inflammatory cytokines play a significant role in the pathophysiology of depression.
Anti-inflammatory agents and trophic cytokines show promise as novel antidepressant strategies.
Further research into neuroinflammation in depression is warranted for biomarker and therapeutic development.