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- W2022559194 abstract "Compelling evidence suggests that inflammation contributes to the development of depression. Many depressed individuals have higher levels of proinflammatory mediators, which appear to interact with many of the pathophysiological domains of depression, including neuroendocrine function, neurotransmitter metabolism, and synaptic plasticity. This is further supported by observation that therapeutic administration of interferon-α (IFN-α) leads to depression in a significant proportion of patients. These findings suggest that targeting proinflammatory cytokines and their signaling pathways may represent a unique therapeutic opportunity to treat depression and related conditions, such as labile anger, irritability, and fatigue." @default.
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- W2022559194 date "2011-11-01" @default.
- W2022559194 modified "2023-10-15" @default.
- W2022559194 title "The Role of Inflammation in the Pathophysiology of Depression: Different Treatments and Their Effects" @default.
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- W2022559194 doi "https://doi.org/10.3899/jrheum.110903" @default.
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