Abstract
Depression is a major cause of worldwide disability. Although its etiology is unclear, for over sixty years the study of its pathophysiology has focused mainly on serotonin (5-HT) and serotonergic neurotransmission. Generally, the study of the pathophysiological processes underpinning depression have led to the appreciation of its complexity, although such study continues to support the role of 5-HT in this disorder.
The aim of this review is to briefly summarize the available findings on 5-HT and depression, with a special focus on alterations in tryptophan (TRP) metabolism that can shift from 5-HT synthesis towards other, potentially neurotoxic, compounds, such as the tryptophan catabolite, quinolinic acid.
The evidence that the TRP shunt may be promoted by stress hormones and proinflammatory cytokines strongly supports the notion that depression should now be considered a systemic disorder that can be triggered by different factors that ultimately target the 5-HT system in vulnerable individuals. In addition, such intriguing findings suggest biochemical targets for novel treatment options in depression.
Keywords: Depression, serotonin, biological markers, tryptophan, tryptophan shunt, kynurenine.
Current Pharmaceutical Design
Title:Depression, Serotonin and Tryptophan
Volume: 22 Issue: 8
Author(s): Liliana Dell’Osso, Claudia Carmassi, Federico Mucci and Donatella Marazziti
Affiliation:
Keywords: Depression, serotonin, biological markers, tryptophan, tryptophan shunt, kynurenine.
Abstract: Depression is a major cause of worldwide disability. Although its etiology is unclear, for over sixty years the study of its pathophysiology has focused mainly on serotonin (5-HT) and serotonergic neurotransmission. Generally, the study of the pathophysiological processes underpinning depression have led to the appreciation of its complexity, although such study continues to support the role of 5-HT in this disorder.
The aim of this review is to briefly summarize the available findings on 5-HT and depression, with a special focus on alterations in tryptophan (TRP) metabolism that can shift from 5-HT synthesis towards other, potentially neurotoxic, compounds, such as the tryptophan catabolite, quinolinic acid.
The evidence that the TRP shunt may be promoted by stress hormones and proinflammatory cytokines strongly supports the notion that depression should now be considered a systemic disorder that can be triggered by different factors that ultimately target the 5-HT system in vulnerable individuals. In addition, such intriguing findings suggest biochemical targets for novel treatment options in depression.
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Cite this article as:
Dell’Osso Liliana, Carmassi Claudia, Mucci Federico and Marazziti Donatella, Depression, Serotonin and Tryptophan, Current Pharmaceutical Design 2016; 22 (8) . https://dx.doi.org/10.2174/1381612822666151214104826
DOI https://dx.doi.org/10.2174/1381612822666151214104826 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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