Abstract
Abstract Substantial evidence exists to indicate a prominent role for chronically elevated levels of cortisol and a dysfunctional feedback system within the hypothalamic–pituitary–adrenal (HPA) axis in major depressive disorder. Chronically elevated cortisol levels are strongly correlated with depression a and normalization of cortisol levels accompanies recovery; failure to normalize predicts relapse or poor recovery. This dysfunction seems to especially link hyperactivity in the system to the role of glucocorticoid receptors. Studies using glucocorticoid synthesis inhibitors or glucocorticoid antagonists in both animals and man have indicated positive effects on the physiological, psychological and pharmacological changes evident in depression. The development of further specific modulators of the glucocorticoid receptors is to be welcomed, however other targets are evident within the HPA axis such as corticotropin-releasing factor (CRF) and vasopressin and may afford equally attractive targets for therapy.
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