From Stress to Inflammation and Major Depressive Disorder: A Social Signal Transduction Theory of Depression

摘要: Major life stressors, especially those involving interpersonal stress and social rejection, are among the strongest proximal risk factors for depression. In this review, we propose a biologically plausible, multilevel theory that describes neural, physiologic, molecular, genomic mechanisms link experiences of social-environmental with internal biological processes drive depression pathogenesis. Central to signal transduction is hypothesis threat adversity up-regulate components immune system involved in inflammation. The key mediators response, called proinflammatory cytokines, can turn elicit profound changes behavior, which include initiation depressive symptoms such as sad mood, anhedonia, fatigue, psychomotor retardation, social-behavioral withdrawal. This highly conserved response critical survival during times actual physical or injury. However, also be activated by modern-day social, symbolic, imagined threats, leading an increasingly phenotype may phenomenon driving pathogenesis recurrence, well overlap several somatic conditions including asthma, rheumatoid arthritis, chronic pain, metabolic syndrome, cardiovascular disease, obesity, neurodegeneration. Insights from thus shed light on important questions how develops, why it frequently recurs, strongly predicted early stress, often co-occurs anxiety certain disease conditions. work suggest new opportunities preventing treating targeting