Neuroinflammation and depression

Abstract An extensive amount of evidence has emerged from animal models and clinical studies that point to a connection between inflammation and depression, mainly based on the association between the presence of some pro-inflammatory cytokines such as TNFα and IL6 and depressive symptoms. The inflammatory hypothesis of depression began to develop, being complementary with the monoamine-related pathophysiology, emphasizing the role of immune-inflammatory dysfunctions present in the disease. Also, during the last two decades, many pieces of evidence have been presented pointing to stress exposure as one of the main sources of inflammation in depression. This chapter reviews the evidence of the coexistence of peripheral low-grade inflammation and neuroinflammation and their effects on brain function and possible causes in depression. Also, we will explore if some neuroinflammation-related mediators might be used as biomarkers of depression. Finally, the current status of the possible use of anti-inflammatory agents in depression is also discussed.