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Depressive disorders pathophysiology

Explain the etiology and pathophysiology of major depressive disorder. [Pg.569]

NEUROTRANSMITTER AND NEUROPEPTIDE SYSTEMS ARE IMPLICATED IN THE PATHOPHYSIOLOGY OF BIPOLAR AND MAJOR DEPRESSIVE DISORDERS 889... [Pg.887]

Unipolar and bipolar depressive disorders in children and adolescents are serious conditions. The pathophysiology of these disorders is poorly understood. The new tools available through neuroimaging techniques will help to unravel the neuroanatomical systems involved in the onset and recurrence of these disorders. There is a need for more developmentally informed predinical research and more studies of the normal development of the neural systems implicated in emotional regulation. [Pg.131]

The relationship between alcohol abuse and suicide has been recognized for many years, with at least one in five suicide victims being intoxicated at the time of their death. Alcohol may lower inhibitions, serving as a precipitant to the act, or the disease of alcoholism itself could be a risk factor. Alcohol also induces biochemical changes (e.g., lowers CSF 5-HIAA and decreases 5-HT2 receptors in the neocortex), similar to changes observed in at least a subset of depressive disorders. Thus, alcohol may aggravate or contribute to the pathophysiology that mediates the depressive syndrome and leads to suicide completions. [Pg.109]

Adapted from Kando, et al. Depressive disorders. In DiPiro JT, et al, eds. Pharmacotherapy A Pathophysiologic Approach. 5th ed. New York McGraw-Hill 2002 1250, with permission. [Pg.85]

Q2 Comment on the pathophysiology of mood swings in manic depressive disorder. [Pg.8]

Cytokine imbalance in the pathophysiology of major depressive disorder. Prog. Neuro-Psychopharmacol. Biol. Psychiatry 94. [Pg.2324]

In summary, many animal of models depressive disorders have been developed, each w ith relative advantages and disadvantages (Nestler et al., 2002). The validity of these models for human depressive disorders continues to be the subject of debate. Probably, this reflects the lack of comprehensive data on the molecular pathophysiology, genetic etiology, and relation to stress in human major depressive disorder. [Pg.499]

Antonijevic lA (2006) Depressive disorders—is it time to endorse different pathophysiologies Psyehoneuroendocrinology 31 1-15. [Pg.491]

While such models of depression are quite useful in conceptualizing the mechanisms behind antidepressant activity, they are assuredly an oversimplification of the actual pathophysiologic process of the disorder. Depression probably involves a complex dysregulation of monoamine systems, and these systems, in turn, modulate and are modulated by other neurobio-logic systems. Thus, the underlying cause of depression may well extend beyond dysfunction of the monoamine system.10... [Pg.571]

Stress is thought to be an important factor in the pathophysiology of depression and anxiety disorders. It seems possible that the reduced stress reactivity of NKl receptor- and tael-deficient mice has contributed to the behavioral phenotypes observed in the animal models of anxiety and depression. [Pg.155]

Ressler KJ, Nemeroff CB (2000) Role of serotonergic and noradrenergic systems in the pathophysiology of depression and anxiety disorders. Depress Anxiety 12 2-19 Reul JMHM, Holsboer F (2002) Corticotropin-releasing hormone receptors 1 and 2 in anxiety and depression. Curr Opin Pharmacol 2 23-33 Rex A, Marsden CA, Fink H (1993) 5-HTlA receptors and changes in extracellular 5-HT in the guinea-pigprefrontal cortex—involvementin aversive behaviour. J Psychopharmacol 7 338-345... [Pg.203]


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See also in sourсe #XX -- [ Pg.1236 ]




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