期刊
EXPERT REVIEW OF NEUROTHERAPEUTICS
卷 12, 期 9, 页码 1143-1161出版社
TAYLOR & FRANCIS LTD
DOI: 10.1586/ERN.12.98
关键词
arachidonic acid; bipolar disorder; C-reactive protein; coronary heart disease; cytokines; immunology; inflammation; major depressive disorder; omega-3 fatty acids; prostaglandins; serotonin
资金
- NIH [MH083924, AG03617]
- NARSAD [MH090250]
- Martek Biosciences Inc.
- Inflammation Research Foundation
- Ortho-McNeil Janssen
- AstraZeneca
- Eli Lilly
Converging translational evidence has implicated elevated immune-inflammatory signaling activity in the pathoetiology of mood disorders, including major depressive disorder and bipolar disorder. This is supported in part by cross-sectional evidence for increased levels of proinflammatory eicosanoids, cytokines and acute-phase proteins during mood episodes, and prospective longitudinal evidence for the emergence of mood symptoms in response to chronic immune-inflammatory activation. In addition, mood-stabilizer and atypical antipsychotic medications downregulate initial components of the immune-inflammatory signaling pathway, and adjunctive treatment with anti-inflammatory agents augment the therapeutic efficacy of antidepressant, mood stabilizer and atypical antipsychotic medications. Potential pathogenic mechanisms linked with elevated immune-inflammatory signaling include perturbations in central serotonin neurotransmission and progressive white matter pathology. Both heritable genetic factors and environmental factors including dietary fatty-acid composition may act in concert to sustain elevated immune-inflammatory signaling. Collectively, these data suggest that elevated immune-inflammatory signaling is a mechanism that is relevant to the pathoetiology of mood disorders, and may therefore represent a new therapeutic target for the development of more effective treatments.
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