The findings determined in rodent models that aberrant Cyclin-dependent kinase-5 activity causes nerve cell death during stroke. "If you inhibit Cyclin-dependent kinase-5, then the vast majority of brain tissue stays alive without oxygen for up to one hour," said Dr James Bibb, senior author of the study from the University of Texas Southwestern Medical Centre.

"This result tells us that Cyclin-dependent kinase-5 is a central player in nerve cell death," said Bibb.

More importantly, development of a Cyclin-dependent kinase-5 inhibitor as an acute neuroprotective therapy has the potential to reduce stroke injury.
"If we could block Cyclin-dependent kinase-5 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. Doing so would have a major impact on health care," Bibb said.
While several pharmaceutical companies worked to develop Cyclin-dependent kinase-5 inhibitors years ago, these efforts were largely abandoned since research indicated blocking Cyclin-dependent kinase-5 long-term could have detrimental effects.

Based on Bibb's research and that of others, Cyclin-dependent kinase-5 has both good and bad effects. When working normally, Cyclin-dependent kinase-5 adds phosphates to other proteins that are important to healthy brain function.

On the flip side, researchers have found that aberrant Cyclin-dependent kinase-5   activity contributes to nerve cell death following brain injury and can lead to cancer.

"Cyclin-dependent kinase-5 regulates communication between nerve cells and is essential for proper brain function. Therefore, blocking Cyclin-dependent kinase-5   for long-term may not be beneficial," Bibb said.

"Until now, the connection between Cyclin-dependent kinase-5 and stroke injury was unknown, as was the potential benefit of acute Cyclin-dependent kinase-5 inhibition as a therapy," said Bibb.

In this study, researchers administered a Cyclin-dependent kinase-5 inhibitor directly into dissected brain slices after adult rodents suffered a stroke, in addition to measuring the post-stroke effects in Cyclin-dependent kinase-5 knockout mice.
"We are not yet at a point where this new treatment can be given for stroke. Nevertheless, this research brings us a step closer to developing the right kinds of drugs," Bibb said.

The study was published in the Journal of Neuroscience.


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