Stroke is a leading cause of long-term disability and death in the United States. A team of researchers — led by Gregory Bix, at Texas A&M College of Medicine, College Station — has identified a way to exploit one of the brain's self-repair mechanisms to protect nerve cells and enhance brain repair in rodent models of stroke. The authors suggest that this approach could provide a nontoxic treatment for stroke.
The most common form of stroke (ischemic stroke) occurs when a blood vessel that brings oxygen and nutrients to the brain becomes clogged, for example with a blood clot, causing nerve cells in the affected area to die rapidly. In their study, Bix and colleagues detected in rodent models of stroke elevated levels of domain V, a naturally occurring fragment of the molecule perlecan, suggesting it might have a natural role in repairing the brain after a stroke. When administered in these models 24 hours after stroke, perlecan domain V protected nerve cells from death and promoted blood vessel growth, a key component of brain repair. The authors therefore suggest that perlecan domain V could provide a therapy that improves stroke outcome by protecting nerve cells and enhancing brain repair.
TITLE: Perlecan domain V is neuroprotective and proangiogenic following ischemic stroke in rodents
AUTHOR CONTACT:
Gregory J. Bix
Texas A&M College of Medicine, College Station, Texas, USA.
Phone: 979.862.7613; Fax: 979.847.9481; E-mail: gjbix@medicine.tamhsc.edu .
View this article at: http://www.jci.org/articles/view/46358?key=975ca4af1b533bd95895
Journal of Clinical Investigation