dc.contributor.author | Hestad, Knut | |
dc.contributor.author | Alexander, Jan | |
dc.contributor.author | Rootwelt, Helge | |
dc.contributor.author | Aaseth, Jan | |
dc.coverage.spatial | Norway | en_US |
dc.date.accessioned | 2023-01-27T10:26:03Z | |
dc.date.available | 2023-01-27T10:26:03Z | |
dc.date.created | 2022-09-09T11:07:58Z | |
dc.date.issued | 2022 | |
dc.identifier.citation | Hestad K, Alexander J, Rootwelt H, Aaseth JO. The Role of Tryptophan Dysmetabolism and Quinolinic Acid in Depressive and Neurodegenerative Diseases. Biomolecules. 2022 Jul 18;12(7):998. doi: 10.3390/biom12070998. | en_US |
dc.identifier.issn | 2218-273X | |
dc.identifier.uri | https://hdl.handle.net/11250/3046809 | |
dc.description.abstract | Emerging evidence suggests that neuroinflammation is involved in both depression and
neurodegenerative diseases. The kynurenine pathway, generating metabolites which may play a role
in pathogenesis, is one of several competing pathways of tryptophan metabolism. The present article
is a narrative review of tryptophan metabolism, neuroinflammation, depression, and neurodegenera tion. A disturbed tryptophan metabolism with increased activity of the kynurenine pathway and
production of quinolinic acid may result in deficiencies in tryptophan and derived neurotransmit ters. Quinolinic acid is an N-methyl-D-aspartate receptor agonist, and raised levels in CSF, together
with increased levels of inflammatory cytokines, have been reported in mood disorders. Increased
quinolinic acid has also been observed in neurodegenerative diseases, including Parkinson’s disease,
Alzheimer’s disease, amyotrophic lateral sclerosis, and HIV-related cognitive decline. Oxidative
stress in connection with increased indole-dioxygenase (IDO) activity and kynurenine formation
may contribute to inflammatory responses and the production of cytokines. Increased formation of
quinolinic acid may occur at the expense of kynurenic acid and neuroprotective picolinic acid. While
awaiting ongoing research on potential pharmacological interventions on tryptophan metabolism, ad equate protein intake with appropriate amounts of tryptophan and antioxidants may offer protection
against oxidative stress and provide a balanced set of physiological receptor ligands. | en_US |
dc.language.iso | eng | en_US |
dc.rights | Navngivelse 4.0 Internasjonal | * |
dc.rights | Navngivelse 4.0 Internasjonal | * |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/deed.no | * |
dc.subject | tryptophan | en_US |
dc.subject | quinolinic acid | en_US |
dc.subject | neurodegeneration | en_US |
dc.subject | NMDA receptor | en_US |
dc.subject | depression | en_US |
dc.subject | Alzheimer | en_US |
dc.subject | Parkinson | en_US |
dc.subject | AIDS | en_US |
dc.subject | antioxidants | en_US |
dc.subject | glutathione | en_US |
dc.title | The Role of Tryptophan Dysmetabolism and Quinolinic Acid in Depressive and Neurodegenerative Diseases | en_US |
dc.title.alternative | The Role of Tryptophan Dysmetabolism and Quinolinic Acid in Depressive and Neurodegenerative Diseases | en_US |
dc.type | Peer reviewed | en_US |
dc.type | Journal article | en_US |
dc.description.version | publishedVersion | en_US |
dc.rights.holder | © 2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https:// creativecommons.org/licenses/by/ 4.0/). | en_US |
dc.subject.nsi | VDP::Medisinske Fag: 700::Klinisk medisinske fag: 750 | en_US |
dc.source.pagenumber | 1-13 | en_US |
dc.source.volume | 12 | en_US |
dc.source.journal | Biomolecules | en_US |
dc.source.issue | 7 | en_US |
dc.identifier.doi | 10.3390/biom12070998 | |
dc.identifier.cristin | 2050250 | |
cristin.ispublished | true | |
cristin.fulltext | original | |
cristin.qualitycode | 1 | |