ATLANTA, May 13 (UPI) — A U.S. study of the clot-busting stroke drug tPA suggests it can act as a neuroprotectant and may be an adaptive response to blood flow reduction.
Emory University School of Medicine researchers said they’ve discovered certain parts of the brains of mice lacking the gene for tissue-type plasminogen activator are more vulnerable to stroke. In addition, tPA can protect neurons in the same part of the brain from the stress of hypoxia — low oxygen.
The drug was introduced as a treatment for acute stroke in the 1990s but there’s been debate about its safety because it can increase the likelihood of hemorrhage and, in some situations, tPA can be a neurotoxin — increasing the permeability of the blood-brain barrier, crossing into brain tissue and generating inflammation.
“tPA is not only a drug, it is a natural protein produced in response to hypoxia,” said Dr. Manuel Yepes, senior author of the study.
He said tPA’s protective properties suggest it may have a role in a process called “ischemic preconditioning,” in which a less-than-lethal stroke can protect against a later repeat. Yepes said tPA’s effects on the blood-brain barrier can be seen as a way to get more blood to a deprived part of the brain.
The study appears in the Journal of Clinical Investigation.
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