Major depressive disorder is the most common mental illness with a complex multifactorial etiology. Abnormalities in the neuroendocrine system are frequently associated with the pathophysiology of this disorder, and among these, alterations in hypothalamic-pituitary-adrenal axis activity and altered levels of cortisol in the context of glucocorticoid resistance are widely observed. Ineffective glucocorticoid signaling can lead to the elevation of inflammation in depressed individuals, where an abnormal communication between the periphery and the central nervous system may provoke neuroinflammation. Activated inflammatory mediators could induce depressive symptoms by directly affecting the brain, modulating the serotonergic system, and/or initiating neurodegenerative processes, through the activation of the kynurenine pathway resulting in a shift toward the production of neurotoxic metabolites. A better understanding of the complex pathophysiological mechanisms underlying the causality and pathogenesis of depression would lead to the development of preventative or personalized treatment strategies in depression.
|Title of host publication||Inflammation and Immunity in Depression|
|Subtitle of host publication||Basic Science and Clinical Applications|
|Publication status||Published - 2018|