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Brain Res. 2015 Aug 18;1617:113-25. doi: 10.1016/j.brainres.2014.06.032. Epub 2014 Jul 5.

Inflammatory cytokine-associated depression.

Author information

1
University of Pittsburgh Medical Center, Western Psychiatric Institute and Clinics, 3811 Ohara Street, Pittsburgh, PA 15213, USA. Electronic address: lotrichfe@upmc.edu.

Abstract

Inflammatory cytokines can sometimes trigger depression in humans, are often associated with depression, and can elicit some behaviors in animals that are homologous to major depression. Moreover, these cytokines can affect monoaminergic and glutamatergic systems, supporting an overlapping pathoetiology with major depression. This suggests that there could be a specific major depression subtype, inflammatory cytokine-associated depression (ICAD), which may require different therapeutic approaches. However, most people do not develop depression, even when exposed to sustained elevations in inflammatory cytokines. Thus several vulnerabilities and sources of resilience to inflammation-associated depression have been identified. These range from genetic differences in neurotrophic and serotonergic systems to sleep quality and omega-3 fatty acid levels. Replicating these sources of resilience as treatments could be one approach for preventing "ICAD". This article is part of a Special Issue entitled SI: Neuroimmunology in Health And Disease.

KEYWORDS:

Cytokine; Depression; Interferon; Interleukin; Mood; Vulnerability

PMID:
25003554
PMCID:
PMC4284141
DOI:
10.1016/j.brainres.2014.06.032
[Indexed for MEDLINE]
Free PMC Article

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