UTSW Finds Inhibitors For Enzyme Could Lead To Treatment For Strokes

Lack of communication never sounded so good.

Research from UT Southwestern suggests that blocking the enzyme Cdk5 could reduce brain damage after a stroke.

Dr. James Bibb, an Associate Professor of Neurology and Neurotherapeutics at UT Southwestern and senior author of the study, led the research concerning the effects of Cdk5 with strokes. According to a statement, the study concluded “aberrant Cdk5 activity causes nerve cell death during stroke.”

“If we could block Cdk5 in patients who have just suffered a stroke, we may be able to reduce the number of patients in our hospitals who become disabled or die from stroke,” Dr. Bibb said in a statement. “Doing so would have a major impact on health care.”

Researchers put Cdk5 inhibitors into dissected rodents’ brains and measured its effects after mice had suffered a stroke.

Cdk5 inhibitors were devised years ago because scientists thought the Cdk5 would influence Alzheimer’s and inhibiting it could become a form of treatment. The drugs were stopped due to their potential long-term effects.

“Cdk5 regulates communication between nerve cells and is essential for proper brain function,” Dr. Bibb said in a statement. “Therefore, blocking Cdk5 long-term may not be beneficial. Until now, the connection between Cdk5 and stroke injury was unknown, as was the potential benefit of acute Cdk5 inhibition as a therapy.”

This new development has not formulated a new treatment for stroke but has shown what types of drugs could be used. Before a clinical trial can be conducted, a systemic drug must be created to conclude Dr. Bibb’s research findings. The only FDA approved drug for a stroke at this time is tPA, a clot-busting drug, and other treatments including neurosurgical procedures.

Other scientists involved in the study were: Dr. Douglas Meyer, lead author and former postdoctoral researcher; Dr. Melissa Torres-Altoro, postdoctoral researcher; Dr. Florian Plattner, instructor; and Dr. Janice Kansy, former postdoctoral researcher. The research was assisted by grants from the National Institute of Health and the Cdk5-inhibitor compound indolinone was supplied through Boehringer Ingelheim pharmaceutical company.

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