摘要
多发性硬化症是一种常见的慢性,致残性自身免疫性神经疾病,主要影响年轻人。在其病理机制中,神经退行性和急性炎症特征均涉及。改善疾病的疗法旨在降低复发率并减缓神经功能的恶化。目前可用的疗法无法发挥神经保护作用,其中大多数疗法与潜在的毒副作用有关,因此,正在进行的研究旨在开发新型候选药物来弥补这些治疗缺口。犬尿氨酸途径已经涉及中枢神经系统的生理过程以及几种神经疾病的病理机制。已经在多发性硬化症中检测到犬尿氨酸途径代谢物的改变,并且已经鉴定了与该代谢途径相关的许多潜在治疗靶标。拉喹莫德是喹啉羧酰胺,显示与犬尿酸的结构相似性,其被证明对减少脑萎缩和残疾进展有有益效果。因此,犬尿氨酸途径对于开发未来用于治疗自身免疫性疾病如多发性硬化症的药物而言是有希望的目标
关键词: 多发性硬化症,拉喹莫德,犬尿氨酸系统,神经保护,神经炎症。
图形摘要
Current Drug Targets
Title:Kynurenine System and Multiple Sclerosis, Pathomechanism and Drug Targets with An Emphasis on Laquinimod
Volume: 19 Issue: 7
关键词: 多发性硬化症,拉喹莫德,犬尿氨酸系统,神经保护,神经炎症。
摘要: Multiple sclerosis is a common chronic, disabling autoimmune neurological disease affecting mainly young adults. In its pathomechanism, neurodegenerative and acute inflammatory characteristics are both involved. Disease-modifying therapies aim to reduce relapse-rate and slow down the deterioration in neurological functions. The currently available therapies fail to exert neuroprotective effects and most of them are associated with potentially toxic side-effects, therefore, ongoing research aims to develop novel drug candidates to cover these therapeutic gaps. The kynurenine pathway has been implicated in both the physiological processes of the central nervous system and in the pathomechanism of several neurological disorders as well. Alterations of the kynurenine pathway metabolites have been detected in multiple sclerosis and a number of potential therapeutic targets related to this metabolic route have been already identified. Laquinimod is a quinoline carboxamide showing structural similarities with kynurenic acid, which proved to have beneficial effects on reduction of brain atrophy and disability progression. The kynurenine pathway is therefore a promising target for the development of future drugs for the treatment of autoimmune diseases such as multiple sclerosis.
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Cite this article as:
Kynurenine System and Multiple Sclerosis, Pathomechanism and Drug Targets with An Emphasis on Laquinimod, Current Drug Targets 2018; 19 (7) . https://dx.doi.org/10.2174/1389450117666161223125417
DOI https://dx.doi.org/10.2174/1389450117666161223125417 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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