Olanzapine and risperidone, for example, are now approved for maintenance treatment in bipolar disorder. Biological predictors During the past years there has been increased interest in the identification of biological predictors of outcome in depression. Among the possible predictors, those derived from neuroendocrine investigations, polysomnographic sleep parameters, genetic variables, and brain imaging techniques have been extensively studied.

Neuroendocrine investigations These predictors can be measured at baseline (ie, after a sufficient drug-withdrawal period) and/or during the Inhibitors,research,lifescience,medical course of treatment. The hypothalamic-pituitary-adrenal (HPA) axis in the Inhibitors,research,lifescience,medical psychobiology of depression has been widely documented (for review see ref 23). Increased Cortisol secretion, failure to suppress Cortisol in response to dexamethasone- the dexamethasone suppression test (DST) and increased corticotropin (ACTH)/cortisol response to the combined dexamethasone/may corticotropin-releasing

hormone (DEX/CRH) test have been consistently associated with severe depression.24-27 It has been hypothesized that this stress axis overdrive is primarily a reflection of abnormal limbic-hypothalamic activation, with chronic increased secretion of corticotropin Inhibitors,research,lifescience,medical releasing hormone (CRH) and consequent excessive adrenal Cortisol secretion linked to impaired negative feedback at the level of the Inhibitors,research,lifescience,medical pituitary corticotroph (ie, decreased type II glucocorticoid receptor function). The Vismodegib buy presence of an abnormal DST or DEX/CRH test indicates the need for a biological treatment, while the initial status of these tests has no predictive value in the choice of given antidepressants.28 Serial DST or combined DEX/CRH test monitoring of depressed patients undergoing drug treatment showed that normalization

Inhibitors,research,lifescience,medical typically precedes or coincides with (rather than follows) clinical recovery, and failure to normalize portends poorly for clinical outcome.29-31 These results suggest that lowering HPA activity – via the restoration of type II glucocorticoid receptor function with a subsequent re-establishment of HPA axis negative feedback-and clinical response are related. The hypothalamic-pituitary-thyroid (HPT) axis is often abnormal in depression. The main Cilengitide abnormality is a chronobiological dysfunction of this axis as reflected by the decreased mean and amplitude of the 24-hour thyroid-stimulating hormone (TSH) secretion32,33 and the blunted TSH test (ie, difference in TSH response between 11 PM and 8 AM protirelin [TRH] tests) in about 80% of depressed inpatients.34 When HPT dysregulation is more pronounced, the 11 PM TRH-TSH test is also abnormal (in about 40% of patients), while the 8 AM TRH-TSH test is blunted in only a minority of inpatients (<20%).