![]() ![]() If the inflammatory response remains unresolved, the chronic release of proinflammatory cytokines can promote pathology, including depression. The main mediators of the inflammatory response, proinflammatory cytokines, such as interleukin (IL)-1β, interleukin (IL)-1 receptor antagonist (RA), interleukin (IL)- 6, tumor necrosis factor (TNF)-α, and interferon (IFN)-γ, have been recently shown to communicate with the brain and affect neurotransmission, neuroendocrine activity, and brain structure and functions, thereby inducing emotional, cognitive, and behavioral changes ( Haroon et al., 2012). Inflammation is a part of the innate immune system’s response to infection or injury. There is growing evidence implicating increased levels of markers of inflammation in the pathogenesis of depressive disorders ( Raison et al., 2006). A multitude of basic research and clinical studies have been performed, with the aim of understanding the interaction between biological, psychological, and environmental factors involved in the etiology of depression. The integration provided aims to contribute toward understanding how biological and psychological processes interact to influence depression outcomes.ĭepression is a highly prevalent mood disorder in modern society and is associated with significant impairments in the patients’ quality of life. ![]() This mini-review summarizes current research on the reciprocal relationships between different types of stressors, emotional attention, inflammation, and depression, and discusses potential neurobiological mechanisms underlying these interactions. Using various designs, recent studies have reported a positive relationship between markers of inflammation and negative attentional bias on behavioral and neural levels, suggesting that the association between inflammation and emotional attention might represent a neurobiological pathway linking stress and depression. Psychological stress triggers inflammatory activity and affective-cognitive changes that play a critical role in the onset, maintenance, and recurrence of depression. Altered attentional processing of emotional information and immunological changes are often precipitated by stressful events. Negative attentional bias, defined as a tendency to direct attention toward negatively valenced information, is one of the core cognitive features of depression and is reliably demonstrated in depressed and vulnerable individuals. Yet, the results are somewhat inconsistent, leading to burgeoning attempts to identify associations between components of innate immune system involved in inflammation and specific symptoms of depression, including attention to emotional information. A growing body of research implicates inflammation in the etiology and pathophysiology of depression. Depression is among the most significant public mental health issues. ![]()
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |