The involvement of immune system activation in the pathophysiology of certain psychiatric disorders is well documented. Inflammatory molecules such as pro-inflammatory cytokines could enhance the activity of the indoleamine 2,3-dioxygenase (IDO) enzyme which is the first rate-limiting enzyme of the tryptophan degradation pathway, the kynurenine pathway. The increased tryptophan degradation could induce serotonin depletion and depressive mood. On the other hand, the downstream metabolites from this pathway, such as 3-hydroxykynurenine, quinolinic acid and kynurenic acid, are neuroactive metabolites which can modulate several neurotransmissions, such as glutamatergic, GABAergic, dopaminergic and noradrenergic neurotransmissions, which in turn induce changes in neuronal-glial network and neuropsychiatric consequences. In this issue, we have revised the previous 'neurodegeneration hypothesis,' which explained the involvement of cytokines and IDO pathway interaction in depression, with a further extended view related to the network beyond IDO, the network between immune molecules, tryptophan metabolites and different neurotransmitters, in depression and other major psychiatric disorders such as schizophrenia, bipolar disorder and childhood psychiatric disorders.
|Number of pages
|Progress in Neuro-Psychopharmacology and Biological Psychiatry
|Published - 2014 Jan 3
Bibliographical noteFunding Information:
The work of Dr. Myint is mainly funded by EU FP7 European Collaborative Research Project ‘MOODINFLAME’ Project No. 22963 and EU FP7 IAAP/Marie Curie Project ‘Psych-AID’ Project No. 286334 and partly supported by Advanced Practical Diagnostics, Belgium . The work of Dr. Kim is supported by Korea University and Korea Health 21 R&D project. The language of the manuscript is checked by a native speaker and professional editor Mr. Jim Burgess.
ASJC Scopus subject areas
- Biological Psychiatry