作者
Andrew D Kraft, Jon M Resch, Delinda A Johnson, Jeffrey A Johnson
发表日期
2007/9/1
期刊
Experimental neurology
卷号
207
期号
1
页码范围
107-117
出版商
Academic Press
简介
Oxidative stress plays a key role in the neuronal loss exhibited in amyotrophic lateral sclerosis (ALS), an event precipitating irreversible muscle atrophy. By crossing ALS mouse models (SODG93A and SODH46RH48Q) with an antioxidant response element (ARE) reporter mouse, we identified activation characteristics of the ARE system throughout the timecourse of motor neuron disease. Surprisingly, the earliest and most significant activation of this genetic sensor of oxidative stress occurred in the distal muscles of mutant SOD mice. The resultant data supports existing hypotheses that the muscle is somehow implicated during the initial pathology of these mice. Subsequently, Nrf2–ARE activation appears to progress in a retrograde fashion along the motor pathway. These data provide timely information concerning the contributions of the Nrf2–ARE pathway in ALS disease progression.
学术搜索中的文章
AD Kraft, JM Resch, DA Johnson, JA Johnson - Experimental neurology, 2007