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Researchers Find Way To Expand Stroke Treatment

By Peter Zuckerman, CONTRIBUTING WRITER

A group of Harvard scientists published findings last month that could lead to significant improvements in the treatment of stroke, the third most common cause of death in the United States.

The study, first published by The Journal of Cerebral Blood Flow and Metabolism, is likely to increase the use of the leading drug for stroke victims.

Striking one American every 45 seconds, according to the American Stroke Association, stroke takes place when a blood vessel that transports oxygen and nutrients to the brain cannot perform its function.

In about 80 percent of cases, the transport failure is due to blood clotting, which blocks vessels. This variety of the disease, known as ischemic stroke, has proven to be difficult to treat because of the risk of blood vessel rupture, or hemorrhage.

In the study, titled “Antiactin Targeted Immunoliposomes Ameliorate Tissue Plasminogen Activator-Induced Hemorrhage After Focal Embolic Stroke,” researchers from the Harvard Medical School (HMS) outline a method that will potentially increase the success of ischemic stroke treatment.

Currently, the only FDA-approved drug for ischemic stroke victims is tissue plasminogen activator (tPA), which is also given to patients who have suffered a heart attack.

However, according to Associate Professor of Radiology Eng H. Lo, a co-author of the study, tPA is used in only 1 to 3 percent of ischemic stroke cases because, if not given in a brief window of time after the stroke, it can cause intracerebral hemorrhage.

Lo said he and his colleagues approached ischemic stroke from an engineering point of view to develop a means of reducing the risk of hemorrhage.

They viewed the network of blood vessels in the brain as a matrix of pipes, he said. And their goal was to seal these pipes so that nothing harmful could leak across the blood-brain barrier, which protects brain tissue.

The researchers found that by sticking antibodies on immunoliposomes, balls of membrane, damaged cells can be sealed.

“Actin in the cells attracts liposomes,” Lo explained. “Liposomes [then] patch the cells.”

But the immunoliposome mechanism may not only be useful for sealing leaks. Xiaoying Wang, an instructor in radiology at HMS and another co-author of the study, noted that the membrane balls could also potentially carry medicine.

Whether the immunoliposomes can adequately perform a second function or not, the procedure’s impact on stroke victims may be far reaching, according to Lo.

“It could make tPA better, make it a hell of a lot better,” said Lo.

And if tPA becomes more powerful, strokes will become less so.

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