"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 concluded."
Washington, June 27 - Giving a ray of hope to heart patients, a research team in the US' University of Texas has suggested that a drug that blocks the action of an enzyme could substantially reduce brain damage if given immediately after a stroke.

If you inhibit (enzyme) Cdk5, then the vast majority of brain tissue stays alive without oxygen for up to one hour, said James Bibb, associate professor of Neurology and Neurotherapeutics at the University of Texas.

The team found that Cdk5 is a central player in nerve cell death following brain injury and can lead to cancer.

Earlier, many scientists thought aberrant Cdk5 activity was pivotal in the development of Alzheimer's disease and that Cdk5 inhibition might be beneficial as a treatment.

Now it is proved that Cdk5 has both good and bad effects.

When working normally, Cdk5 adds phosphates to other proteins that are important to healthy brain function.

Cdk5 regulates communication between nerve cells and is essential for proper brain function. Therefore, blocking Cdk5 long-term may not be beneficial, Bibb noted.

Until now, the connection between Cdk5 and stroke injury was unknown, as was the potential benefit of acute Cdk5 inhibition as a therapy, he added.

The researchers administered a Cdk5 inhibitor directly into dissected brain parts after adult rodents suffered a stroke, in addition to measuring the post-stroke effects in Cdk5 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 concluded.

The findings appeared in the Journal of Neuroscience.


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