Experimental drug holds post-stroke promise

Posted: Published on March 2nd, 2012

This post was added by Dr Simmons

TORONTO Newly reported Canadian research is holding out hope that a treatment for minimizing the damage done by the most common type of stroke could be on the horizon.

A Toronto-based research team is reporting that an experimental drug significantly reduced brain damage and post-stroke impairment when used in macaque monkeys in which strokes were induced.

The report, in the journal Nature, makes no reference to use of the drugs in humans.

But at an international stroke conference in New Orleans in early February, the team presented preliminary data of a Phase II human trial in which the drug was reported to be quite favourable. Larger and more expensive Phase III trials are needed to gain regulatory approval to bring drugs to market.

The new report, which lays out data from a series of experiments in monkeys, is being greeted with enthusiasm laced with caution.

Researchers have tried for more than half a century to find a drug or therapy to protect the brain from the cascade of damage seen after an ischemic stroke, the type caused by a blockage of blood to the brain. About 85 per cent of strokes are the result of clots blocking blood flow, depriving the brain of oxygen.

More than 1,000 experimental treatments to protect the brain after this type of stroke have been tried in cell culture, in mice and in rats. Time after time hopes have been dashed.

Everyone has cured rats of stroke. And no one has managed to cure or to help with neuroprotection in human stroke, said Dr. Michael Tymianski, senior author of the paper and principle investigator on this drug, known at this point as Tat-NR2B9c.

In fact, the history of repeated failures in the search for neuroprotector drugs has led some to conclude the human brain is too complex to be shielded in this way.

Currently there is only one treatment available for ischemic stroke. Drugs that break up the clot can minimize the damage done. But clot busters must be used within a small window; if given later than 4 hours after a stroke they have no effect. That limitation gave rise to the maxim used in describing the urgency of stroke care: Time is brain.

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Experimental drug holds post-stroke promise

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