期刊
TRENDS IN IMMUNOLOGY
卷 27, 期 1, 页码 24-31出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.it.2005.11.006
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资金
- NCRR NIH HHS [M01 RR000039] Funding Source: Medline
- NHLBI NIH HHS [R01 HL073921] Funding Source: Medline
- NIMH NIH HHS [R01 MH067990, K05 MH069124, R01 MH075102, R01 MH060723, R01 MH047674] Funding Source: Medline
- NATIONAL CENTER FOR RESEARCH RESOURCES [M01RR000039] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL073921] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF MENTAL HEALTH [R01MH047674, R01MH067990, R01MH060723, K05MH069124, R01MH075102] Funding Source: NIH RePORTER
Increasing amounts of data suggest that inflammatory responses have an important role in the pathophysiology of depression. Depressed patients have been found to have higher levels of proinflammatory cytokines, acute phase proteins, chemokines and cellular adhesion molecules. In addition, therapeutic administration of the cytokine interferon-a leads to depression in up to 50% of patients. Moreover, proinflammatory cytokines have been found to interact with many of the pathophysiological domains that characterize depression, including neurotransmitter metabolism, neuroendocrine function, synaptic plasticity and behavior. Stress, which can precipitate depression, can also promote inflammatory responses through effects on sympathetic and parasympathetic nervous system pathways. Finally, depression might be a behavioral byproduct of early adaptive advantages conferred by genes that promote inflammation. These findings suggest that targeting proinflammatory cytokines and their signaling pathways might represent a novel strategy to treat depression.
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