July 11, 2011 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.
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- Boyeon Lee, Douglas Clarke, Abraham Al Ahmad, Michael Kahle, Christi Parham, Lisa Auckland, Courtney Shaw, Mehmet Fidanboylu, Anthony Wayne Orr, Omolara Ogunshola, Andrzej Fertala, Sarah A. Thomas, Gregory J. Bix. Perlecan domain V is neuroprotective and proangiogenic following ischemic stroke in rodents. Journal of Clinical Investigation, 2011; DOI: 10.1172/JCI46358
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