有可能革新ALS疗法的新发现

若水之媚

Sept. 21, 2011 at 12:06 AM

2011年9月21日上午12:06

VANCOUVER, British  Columbia, Sept. 21 (UPI) -- A link between prions and theneurodegenerative disease amyotrophic lateral sclerosis might lead to newtreatments, Canadian researchers say.

温哥华，不列颠哥伦比亚省，9月21日。加拿大研究人员宣布：朊病毒和ALS之间的关联有可能衍生出新的疗法。

Dr. NeilCashman, academic director of the VancouverCoastal HealthALS Center,and colleagues at the University of British Columbia, saidthe study demonstrates that the SOD1 protein -- which has been shown to beimplicated in the ALS disease process -- exhibits prion-like properties. Aprion is an infectious agent composed of protein in a misfolded form.

温哥华健康ALS中心学术主任Neil Cashman博士及其不列颠哥伦比亚大学的同事表示：研究发现：与ALS疾病进程有关的SOD1蛋白，表现出阮病毒状的属性。朊病毒是是由错误折叠的蛋白构成的传染性病原体。

The researchers foundthat SOD1 participates in a process called template-directed misfolding, whichrefers to the coercion of one protein by another protein to change shape andaccumulate in large complexes in a fashion similar to the process underlyingprion diseases.

研究人员发现：SOD1参与一种被称为template-directed（模板指导）错误折叠的过程。该过程涉及一种蛋白强制改变另一种蛋白的形状，并堆积为大的复合物。该过程与潜在的阮病毒疾病过程，在方式上有相似之处。。

The discovery issignificant as it opens the door to novel approaches to the treatment of ALS --also known as Lou Gehrig's disease -- Cashman said.

Cashman说：这一发现意义重大，为寻找新的ALS疗法开辟了方向。

"Our work hasidentified a specific molecular target, which when manipulated halts theconversion of the SOD1 protein to a misfolded, disease-causing form," Cashmansaid in a statement. "This discovery is a first-step toward thedevelopment of targeted treatments that may stop progression of ALS."

“我们的工作确定一个特定的分子标靶，那就是控制性终止SOD1蛋白转换为错误折叠的致病形式” Cashman在一份声明中说，“这一发现向开发出可能终止ALS发展的疗法方向迈出了第一步”

The study was publishedin the Proceedings of the National Academy of Sciences.

研究结果发表在《国家科学学报》上。

内容来源于：http://www.upi.com/Health_News/2011/09/21/Discovery-may-revolutionize-ALS-treatment/UPI-79201316578009/，病友明年幸福--江苏提供资讯。

祈盼奇迹

好啊，，不错、、、、  

litianguang

谢谢楼主