Public release date: 17-Jul-2012 [ | E-mail | Share ]
Contact: Quinn Eastman qeastma@emory.edu 404-727-7829 Emory University
Even when its clot-dissolving powers are removed, the stroke drug tPA can still protect brain cells from the loss of oxygen and glucose induced by a stroke, researchers have discovered.
The finding suggests that a modified version of tPA could provide benefits to patients who have experienced a stroke, without increasing the risk of bleeding.
The results will be published in the Journal of Neuroscience.
"We may have been giving the right medication, for the wrong reason," says senior author Manuel Yepes, MD, associate professor of neurology at Emory University School of Medicine. "tPA is more than a clot-busting drug, it functions naturally as a neuroprotectant,"
The co-first authors of the paper are postdoctoral fellows Fang Wu and Jialing Wu from the Department of Neurology, and Andrew Nicholson from the Department of Radiology and Imaging Sciences.
tPA was introduced as a treatment for acute stroke in the 1990s. Doctors have debated its effectiveness and safety ever since, because it can increase the likelihood of deadly hemorrhage. Many people experiencing a stroke do not receive tPA because of time constraints or other contraindications.
"tPA is supposed to be administered within the first 3-4.5 hours of the onset of the stroke," Yepes says. "Otherwise there is no beneficial effect and instead there is an increase in the risk of hemorrhagic transformation."
Long before tPA ever became a drug, tPA was a protein produced by several tissues in the body, including brain cells. One of its functions is to convert the inactive protein plasminogen into the enzyme plasmin, which breaks down clots. Yepes' team has been studying tPA's additional functions beyond acting on plasminogen.
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Modified tPA could be effective stroke treatment without bleeding risk