%0 Journal Article
%@ 1472-8222
%A  Boros Fanni Annamária
%A  Klivényi Péter
%A  Toldi József
%A  Vécsei László
%A Élettani, Szervezettani és Idegtudományi Tanszék SZTE / TTIK / BI ÉSZIT [2016-],
%A Neurológiai Klinika SZTE / ÁOK NeurK [2000-],
%A MTA-SZTE Idegtudományi Kutatócsoport SZTE / ÁOK / NeurK [2012-],
%D 2019
%F publicatio:15735
%J EXPERT OPINION ON THERAPEUTIC TARGETS
%N 1
%P 39-51
%T Indoleamine 2,3-dioxygenase as a novel therapeutic target for Huntington’s disease
%U http://publicatio.bibl.u-szeged.hu/15735/
%V 23
%X Introduction: Huntington’s disease (HD) is an autosomal dominant, neurodegenerative disorder. Despite the severe motor, psychiatric and cognitive symptoms and the great socioeconomic burden caused by the disease, available treatment is mainly symptomatic. The kynurenine pathway (KP) is the main metabolic route of tryptophan degradation, in the course of which several neuroactive compounds are generated. The imbalance of the neurotoxic and neuroprotectant metabolites can lead to excitotoxicity and overproduction of reactive oxygen species, which both contribute to the progression of HD. Indoleamine 2,3-dioxygenase 1 (IDO1) is a key enzyme of the KP that has various immune modulatory roles. Areas covered: Current knowledge of the involvement of KP in HD pathogenesis with a particular focus on IDO1. By reviewing the diverse roles of the enzyme in kynurenine production, immune modulation, and serotonin metabolism, we elucidate the factors that make this enzyme a therapeutic target. Expert opinion: Due to the complexity of HD and the various effects that IDO1 exerts, targeting this enzyme, while highly profitable, may be a great challenge. Through IDO1 activity, neurodegeneration, inflammatory processes and depressive symptoms, often related to HD, can be modulated. Ongoing trials of IDO1 inhibitors in other areas of medicine offer advantages for initiating approaches toward this enzyme as a therapeutic target. © 2018, © 2018 Informa UK Limited, trading as Taylor & Francis Group.
%Z Department of Neurology, Albert Szent-Györgyi Clinical Center, Faculty of Medicine, University of Szeged, Szeged, Hungary   Department of Physiology, Anatomy and Neuroscience, Faculty of Science and Informatics, University of Szeged, Szeged, Hungary   MTA-SZTE Neuroscience Research Group of the Hungarian Academy of Sciences and the University of Szeged, Szeged, Hungary   Export Date: 10 December 2018   Article in Press   CODEN: EOTTA   Correspondence Address: Vécsei, L.; Albert Szent-Györgyi Medical Center, Faculty of Medicine, University of Szeged, P.O. Box: 427, Hungary; email: vecsei.laszlo@med.u-szeged.hu Funding Agency and Grant Number: Economic Development and Innovation Operational Programme [GINOP-2.3.2-15-2016-00034]; Hungarian Brain Research Program [2017-1.2.1-NKP-2017-00002 NAP VI/4]; Ministry of Human Capacities, Hungary [20391-3/2018/FEKUSTRAT]; MTA-SZTE Neuroscience Research Group of the Hungarian Academy of Sciences; University of Szeged             Funding text: This paper was not funded. The current work was supported by Economic Development and Innovation Operational Programme - GINOP-2.3.2-15-2016-00034, Hungarian Brain Research Program - Grant No. 2017-1.2.1-NKP-2017-00002 NAP VI/4, Ministry of Human Capacities, Hungary grant 20391-3/2018/FEKUSTRAT and the MTA-SZTE Neuroscience Research Group of the Hungarian Academy of Sciences and the University of Szeged. Department of Neurology, Albert Szent-Györgyi Clinical Center, Faculty of Medicine, University of Szeged, Szeged, Hungary                         Department of Physiology, Anatomy and Neuroscience, Faculty of Science and Informatics, University of Szeged, Szeged, Hungary                         MTA-SZTE Neuroscience Research Group of the Hungarian Academy of Sciences and the University of Szeged, Szeged, Hungary                         Export Date: 27 December 2018                         CODEN: EOTTA                         Correspondence Address: Vécsei, L.; Albert Szent-Györgyi Medical Center, Faculty of Medicine, University of Szeged, P.O. Box: 427, Hungary; email: vecsei.laszlo@med.u-szeged.hu                         Chemicals/CAS: 4 amino n (3 chloro 4 fluorophenyl) n' hydroxy 1,2,5 oxadiazole 3 carboximidamide, 914471-09-3; huntingtin, 191683-04-2; indoleamine 2,3 dioxygenase; indoximod, 110117-83-4; kynurenic acid, 492-27-3; kynurenine, 16055-80-4, 343-65-7; memantine, 19982-08-2, 41100-52-1, 51052-62-1; nitric oxide, 10102-43-9; nitric oxide synthase, 125978-95-2; polyglutamine, 26700-71-0, 69864-43-3; quinolinic acid, 89-00-9; remacemide, 111686-79-4; serotonin, 50-67-9; tryptophan, 6912-86-3, 73-22-3                         Tradenames: incb 24360; jm 6; ro 61 8048