Implications for the Kynurenine Pathway and Quinolinic Acid in Amyotrophic Lateral Sclerosis

Implications for the Kynurenine Pathway and Quinolinic Acid in Amyotrophic Lateral Sclerosis
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DOI:
10.1159/000089622
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发表时间:
2005-01-01
影响因子:
3
通讯作者:
Brew, Bruce J.
Brew, Bruce J.
中科院分区:
医学4区
文献类型:
--
作者:
Guillemin, Gilles J.;Meininger, Vincent;Brew, Bruce J.

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犬尿氨酸途径(KP)是L-色氨酸催化剂的主要途径,导致产生几种神经生物学活性分子。其中之一是兴奋毒素喹啉酸(QUIN),已知其参与几种主要炎性神经系统疾病的发病机制。在肌萎缩侧索硬化症(ALS)中,运动神经元的变性与慢性和局部炎症(存在活化的小胶质细胞和星形胶质细胞)相关。有新的证据表明,KP在ALS中很重要。最近,我们证明QUIN在ALS患者的血清和CSF中显著增加。此外,大多数与QUIN毒性相关的因素都存在于ALS中,这意味着QUIN可能在ALS的神经发病机制中发挥重要作用。本文详细介绍了潜在的作用,KP在ALS和先进的可测试的假设模型。版权所有(C)2005 S. Karger AG,巴塞尔
The kynurenine pathway (KP) is a major route of L-tryptophan catabolism leading to production of several neurobiologically active molecules. Among them is the excitotoxin quinolinic acid (QUIN) that is known to be involved in the pathogenesis of several major inflammatory neurological diseases. In amyotrophic lateral sclerosis (ALS) degeneration of motor neurons is associated with a chronic and local infl ammation (presence of activated microglia and astrocytes). There is emerging evidence that the KP is important in ALS. Recently, we demonstrated that QUIN is significantly increased in serum and CSF of ALS patients. Moreover, most of the factors associated with QUIN toxicity are found in ALS, implying that QUIN may play a substantial role in the neuropathogenesis of ALS. This review details the potential role the KP has in ALS and advances a testable hypothetical model. Copyright (C) 2005 S. Karger AG, Basel