Neuroendocrine Abnormalities in Major Depression: An Insight Into Glucocorticoids, Cytokines, and the Kynurenine Pathway

TY - CHAP

T1 - Neuroendocrine Abnormalities in Major Depression: An Insight Into Glucocorticoids, Cytokines, and the Kynurenine Pathway

AU - Nikkheslat, Naghmeh

AU - Pariante, Carmine Maria

AU - Zunszain, Patricia Ana

PY - 2018

Y1 - 2018

N2 - 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.

AB - 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.

M3 - Chapter

SP - 45

EP - 60

BT - Inflammation and Immunity in Depression

ER -