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주요우울증에서 사이토카인-세로토닌 상호작용에 의한 신경변성 가설A Neurodegenerative Hypothesis of Cytokine-Serotonin Interaction in Major Depression

Other Titles
A Neurodegenerative Hypothesis of Cytokine-Serotonin Interaction in Major Depression
Authors
김용구
Issue Date
Jul-2004
Publisher
대한신경정신의학회
Keywords
Serotonin; Cytokine; Neurogenesis; Neurodegeneration; IDO; Depression; 세로토닌; 사이토카인; 신경조직발생; 신경변성; 우울증.
Citation
신경정신의학, v.43, no.4, pp.386 - 392
Indexed
KCI
OTHER
Journal Title
신경정신의학
Volume
43
Number
4
Start Page
386
End Page
392
URI
https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/32204
ISSN
1015-4817
Abstract
A growing body of evidence suggests that major depression is associated with increased productions of pro-inflammatory cytokines such as IL-1, IL-6, IL-12 or TNF-alpha and increased concentrations of prostaglandin E2 and negative-regulatory cytokines such as IL-4 or IL-10. In major depression, interactions among brain 5-HT levels, the activity of its autoreceptors, and that of postsynaptic receptors play a critical role in mood changes and depression. Recently, the link between cytokines and serotonergic turnover has been explored. Cytokines such as IL-1, IL-2 and IFN-gamma reduce the production of 5-HT by stimulating the activity of indoleamine-2,3 dioxygenase (IDO), an enzyme which convert tryptophan, the precursor of 5-HT to kynurenine. The kynurenine is metabolized into quinolinic acid (quinolinate) and kynurenic acid (kynurenate), an excitotoxic NMDA receptor agonist and the antagonist of three ionotropic excitotatory aminoacid receptors, respectively. The cytokineserotonin interaction through IDO that leads to the challenge between quinolinate and kynurenate in the brain may finally induce the neurodegeneration in depression. The neurodegeneration hypothesis of depression can explain how people cope with psychological or physical stress at different stages according to severity and duration of stress and why major depression develops. (J Korean Neuropsychiatr Assoc 2004;43(4):386-392)
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