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왜 다양한 항우울제가 필요한가?

Who Do We Need Diverse Antidepressnats?

김용구|윤호경
대한신경정신의학회 (Korean Neuropsychiatric Association)|2008.01|신경정신의학 (JOURNAL OF THE KOREAN NEUROPSYCHIATRIC ASSOCIATION)|제47권 제1호|pp. 11-21

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항우울제·신경생물학·단가아민·사이토카인·우울증.Antidepresant· Neurobiology· Monoamine· Cytokine· Depression.
주제분류정신과학

초록

Depression is a chronic, recurring and potentially life-threatening illness. Depression is a syndrome notable for heterogeneity of its clinical presentation, treatment responsiveness, neurobiology, and genetics. The highly variable compilation of symptoms that is used to define depression, and the highly variable course of the illness and its response to various treatments, indicate that depression subsumes numerous disease states of distinct etiology, and perhaps distinct pathophysiology. Current understanding of the mechanisms of pharmacotherapy for depression is characterized by the emphasis on increasing synaptic availability of serotonin, noradrenaline, and possibly dopamine, while minimizing side effects. This is unfortunate, because less than half of individuals with depression show full remission in response to these mechanisms. While current pharmacotherapies target monoaminergic systems, distinct neurobiological underpinnings and other systems are likely involved in the pathogenesis of depression. Recently, several promising hypotheses of depression and antidepressant action have been formulated. These hypotheses are largely based on dsyregulation of neural plasticity, CREB, BDNF, corticotropin-releasing factor, glucocorticoid, hypothalamic-pituitary adrenal axis and cytokines. Based on these new theories and hypotheses of depression, a number of new and novel agents show a considerable promise for refining treatment options for depression. In this article, we provide an overview of the mechanisms of action of currently available antidepressant treatments. We then provide a progress report on some of the most promising current strategies. (J Korean Neuropsychiatr Assoc 2008;47(1):11-21)

Abstract

Depression is a chronic, recurring and potentially life-threatening illness. Depression is a syndrome notable for heterogeneity of its clinical presentation, treatment responsiveness, neurobiology, and genetics. The highly variable compilation of symptoms that is used to define depression, and the highly variable course of the illness and its response to various treatments, indicate that depression subsumes numerous disease states of distinct etiology, and perhaps distinct pathophysiology. Current understanding of the mechanisms of pharmacotherapy for depression is characterized by the emphasis on increasing synaptic availability of serotonin, noradrenaline, and possibly dopamine, while minimizing side effects. This is unfortunate, because less than half of individuals with depression show full remission in response to these mechanisms. While current pharmacotherapies target monoaminergic systems, distinct neurobiological underpinnings and other systems are likely involved in the pathogenesis of depression. Recently, several promising hypotheses of depression and antidepressant action have been formulated. These hypotheses are largely based on dsyregulation of neural plasticity, CREB, BDNF, corticotropin-releasing factor, glucocorticoid, hypothalamic-pituitary adrenal axis and cytokines. Based on these new theories and hypotheses of depression, a number of new and novel agents show a considerable promise for refining treatment options for depression. In this article, we provide an overview of the mechanisms of action of currently available antidepressant treatments. We then provide a progress report on some of the most promising current strategies. (J Korean Neuropsychiatr Assoc 2008;47(1):11-21)

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