Depression can originate from changes in tryptophan availability, caused by activation of the kynurenine pathway (KP) as a result of inflammation. Alterations in the KP and the changing levels of its metabolites have recently been considered to be factors contributing to the pathogenesis of depression. The key molecular mediator which induces the conversion of tryptophan into kynurenine is indoleamine-2,3-dioxygenase. Following its activation, both the production of neurotoxic compounds and the diminished peripheral accessibility of tryptophan are regarded as essential steps in the pathophysiological processes. The aim of this review is to survey the role of the KP in depression and its relationships with cognitive functions.
|Translated title of the contribution||Kynurenines in cognitive functions: Their possible role in depression|
|Number of pages||6|
|Publication status||Published - Dec 1 2012|
ASJC Scopus subject areas
- Neuropsychology and Physiological Psychology
- Pharmacology, Toxicology and Pharmaceutics(all)
- Clinical Neurology