Abstract
Increasing evidence of pro-inflammatory mediator expression in major depressions indicate that inflammatory changes may play a role. If this is true, the efficacy of antidepressants may be partially attributable to suppression of inflammation. Various types of antidepressants can suppress serum and plasma levels of pro-inflammatory mediators in patients with major depression. Therefore they can inhibit the production of pro-inflammatory mediators by immune cells. These include glial cells, which are the main sources and targets of cytokines in the brain. This review summarizes the evidence showing that antidepressants have an anti-inflammatory potential. The putative mechanisms are also discussed. Because of the anti-inflammatory effects of antidepressants, they might also act as preventives for neurodegenerative dementias including Alzheimer's disease, where the pathogenesis involves chronic inflammation associated with activated microglia.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Adjuvants, Immunologic
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Alzheimer Disease / prevention & control*
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Amyloid beta-Peptides / analysis*
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Animals
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Anti-Inflammatory Agents
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Antidepressive Agents / pharmacology
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Antidepressive Agents / therapeutic use*
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Antioxidants / pharmacology
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Cells, Cultured
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Cognition Disorders / prevention & control
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Cytokines / physiology
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Dementia / etiology*
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Depressive Disorder / prevention & control*
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Depressive Disorder, Major / prevention & control
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Humans
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Inflammation / etiology
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Inflammation Mediators / metabolism
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Interferon-gamma / pharmacology
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Microglia / drug effects*
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Microglia / pathology
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Nerve Regeneration*
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Neuroglia / drug effects
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Neurons / drug effects
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Neurons / metabolism
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Oxidative Stress / drug effects
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Oxidative Stress / physiology
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Prions
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Stress, Psychological
Substances
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Adjuvants, Immunologic
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Amyloid beta-Peptides
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Anti-Inflammatory Agents
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Antidepressive Agents
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Antioxidants
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Cytokines
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Inflammation Mediators
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Prions
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Interferon-gamma