Department of Neurology, Albert Szent-Györgyi Clinical Centre, University of Szeged, Szeged, Hungary.
J Cell Mol Med. 2011 Apr;15(4):701-17. doi: 10.1111/j.1582-4934.2010.01237.x.
Parkinson's disease (PD) and Huntington's disease (HD) are progressive chronic neurodegenerative disorders that are accompanied by a considerable impairment of the motor functions. PD may develop for familial or sporadic reasons, whereas HD is based on a definite genetic mutation. Nevertheless, the pathological processes involve oxidative stress and glutamate excitotoxicity in both cases. A number of metabolic routes are affected in these disorders. The decrease in antioxidant capacity and alterations in the kynurenine pathway, the main pathway of the tryptophan metabolism, are features that deserve particular interest, because the changes in levels of neuroactive kynurenine pathway compounds appear to be strongly related to the oxidative stress and glutamate excitotoxicity involved in the disease pathogenesis. Increase of the antioxidant capacity and pharmacological manipulation of the kynurenine pathway are therefore promising therapeutic targets in these devastating disorders.
帕金森病（PD）和亨廷顿病（HD）是进行性慢性神经退行性疾病，伴有运动功能的严重损伤。PD 可能由家族或散发性原因引起，而 HD 则基于明确的基因突变。然而，在这两种情况下，病理过程都涉及氧化应激和谷氨酸兴奋性毒性。这些疾病还会影响许多代谢途径。抗氧化能力下降和色氨酸代谢的主要途径——犬尿氨酸途径的改变，是值得特别关注的特征，因为神经活性犬尿氨酸途径化合物水平的变化似乎与疾病发病机制中涉及的氧化应激和谷氨酸兴奋性毒性密切相关。因此，增加抗氧化能力和对犬尿氨酸途径的药理学干预是这些破坏性疾病有前途的治疗靶点。
