Early Research Shows Benefit for Enzyme Inhibitor in Stroke Victims

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Minutes and seconds can make a difference in the amount of brain damage suffered by a stroke patient, but now scientists have shown that medication can significantly help limit the damage.

Minutes and seconds can make a difference in the amount of brain damage suffered by a stroke patient, but now scientists have shown that medication can significantly help limit the damage.

According to the study published in a recent edition of the Journal of Neuroscience, patients who receive a drug that blocks the enzyme Cdk5 shortly after a stroke can get the extra help needed to maintain normal brain function.

Senior study author James Bibb, MD, Associate Professor of Neurology and Neurotheraputics at the University of Texas Southwestern Medical Center, said the results were encouraging and could aid patients during the key time following a stroke.

“If you inhibit Cdk5, then the vast majority of brain tissue stays alive without oxygen for up to one hour,” he reported. “This result tells us that Cdk5 is a central player in nerve cell death.”

By continuing to work with the enzyme blocker and getting it to patients as quickly as possible after a stroke, Bibb said doctors will be able to “reduce the number of patients in our hospitals who become disabled or die from stroke,” which he noted will have a "major impact on healthcare.”

One potential complication for Bibb’s research is the fact that past studies of Cdk5 inhibitors showed some detrimental effects. During that time, the medication was seen as a possible drug to help patients with Alzheimer’s disease.

For his part, Bibb said the research showed positives and negatives with the potential treatment. Intended to add phosphates to other proteins, aberrant Cdk5 has also contributed to nerve cell death in patients with brain injuries, and it has also lead to cancer.

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

Since Bibb’s study involved injecting the inhibitor right into the brain of adult rodents after a stroke, he noted the effect of the drug on humans has yet to be fully determined.

“We are not yet at a point where this new treatment can be given for a stroke,” he said. “Nevertheless, this research brings us a step closer to developing the right kind of drugs.”

According to Bibb, the next steps in the research will involve several steps, including the development of a pill that could eventually be given to human patients.

“We first need to know what mechanisms underlie the disease before targeted treatments can be developed that will be effective,” he added. “As no Cdk5 blocker exists that works in a pill form, the next step will be to develop a systemic drug that could be used to confirm the study’s results and lead to a clinical trial at later stages.”

The study was supported by grants from the National Institutes of Health (NIH), while Boehringer Ingelheim provided the enzyme-inhibiting compound indolinone.

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