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Cytokines sing the blue: inflammation and the pathogenesis of depression
Raison CL, Capuron L, Miller AH
Trends in Immunology 2006; 27:24-31.
Summary
This is a review of evidence from one of the 'modeling' studies conducted by the CDC CFS collaborative research group. Modeling studies conducted collaboratively with research group investigators from Emory University measure immune and neuroendocrine parameters and sleep, metabolism, mood, and cognitive responses to interferon (IFN)-α therapy for hepatitis C virus (HCV). IFN-α is a powerful immune modulator, and patients who receive IFN-α develop a CFS-like illness. Insights gained from studies of IFN-α have helped us to interpret results from field studies of CFS. This review article discusses means by which inflammation may contribute to the cause of CFS.
Abstract
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.
Page last modified on October 24, 2007
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