Cytokine-serotonin interaction through IDO: a neurodegeneration hypothesis of depression
- Authors
- Myint, AM; Kim, YK
- Issue Date
- Nov-2003
- Publisher
- CHURCHILL LIVINGSTONE
- Keywords
- NECROSIS-FACTOR-ALPHA; INDOLEAMINE 2; 3-DIOXYGENASE ACTIVITY; HUMAN MONONUCLEAR PHAGOCYTES; CENTRAL-NERVOUS-SYSTEM; MAJOR DEPRESSION; QUINOLINIC ACID; TRYPTOPHAN 2; 3-DIOXYGENASE; PSYCHOLOGICAL STRESS; RECEPTOR ANTAGONIST; KYNURENINE PATHWAY
- Citation
- MEDICAL HYPOTHESES, v.61, no.5-6, pp 519 - 525
- Pages
- 7
- Indexed
- SCIE
SCOPUS
- Journal Title
- MEDICAL HYPOTHESES
- Volume
- 61
- Number
- 5-6
- Start Page
- 519
- End Page
- 525
- URI
- https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/21004
- DOI
- 10.1016/S0306-9877(03)00207-X
- ISSN
- 0306-9877
1532-2777
- Abstract
- There are different theories and hypotheses related to the aetiology of depression. The interaction between brain 5-HT level and the activity of its autoreceptors plays a role in mood changes and depression. In major depression, activation of the inflammatory response system (IRS) and, increased concentrations of proinflammatory cytokines, prostaglandin E2 and negative immuno-regulatory cytokines in peripheral blood have been reported. Recently, pro-inflammatory cytokines have been found to have profound effects on the metabolism of brain serotonin through the enzyme indoleamine-2,3-dioxygenase (IDO) that metabolizes the tryptophan, the precursor of 5-HT to neurodegenerative quinolinate and neuroprotective kynurenate. The cytokine-serotonin interaction that leads to the challenge between quinolinate and kynurenate in the brain explains the neurodegeneration hypothesis of depression. (C) 2003 Elsevier Ltd. All rights reserved.
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Collections - 2. Clinical Science > Department of Psychiatry > 1. Journal Articles
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