Inflammation and depression Sample Clauses

Inflammation and depression. There is a substantial amount of clinical evidence that supports the notion that the immune system is activated in depressed patients, and that this activation plays a role in disease progression as well as the ameliorating effects of antidepressant therapy (A Xxxxxx, Xxxxxxx, & Xxxxxx, 2009; Xxxxxx et al., 2006). Recent meta-analyses revealed that patients with MDD exhibit elevated peripheral blood inflammatory biomarkers, most commonly, proinflammatory cytokines IL-1, IL-6 and TNF-α, and CRP (Xxxxxxx et al., 2010; Y Xxx, Xx, & Xxx, 2012). Levels of numerous other cytokines, such as IL-1 and monocyte chemoattractant protein 1 (MCP-1), have also been shown to be raised (Xxxxxxxx et al., 2001). Furthermore, studies have demonstrated that such elevated levels of inflammatory biomarkers can be reversed by effective antidepressant treatment (Lanquillon, Krieg, Bening-Abu-Shach, & Xxxxxx, 2000). Work from animal studies has also demonstrated that treatment with proinflammatory cytokines induces depressive-like behaviours in rodents (Anisman, 2009). More direct evidence that inflammation is involved in the pathogenesis of depression comes from studies examining the effects of IFN-α treatment. It has been observed that within 3 months, up to 50% of patients undergoing such treatment acquire depression symptoms which meet criteria for a diagnosis of MDD (Xxxxxxxxx, Xxxxxx, et al., 2001; Xxxxxx et al., 2005). These studies form the foundation for the theory of cytokine-mediated inflammatory processes in the pathogenesis of depression. Accordingly, inflammation is argued to contribute to a state of HPA axis dysfunction by promoting GC resistance (A Xxxxxx, 2009; Xxxx et al., 2007; Xxxxxxxx et al., 2011), through a process of cytokine-induced functional impairment of the GR (. Xxxxxx & Xxxxxx, 2006; Xxxx, Xx, & Xxxxxx, 2004).