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Estrogen, estrogen-like drugs' ability to protect brain after stroke under study

anding the steps to cell death and how these types of drugs alter the steps, "you could design a SERM that could act on a particular tissue and have the desired effect," says Dr. Brann.

The potential of these substances to thwart the pro-death cycle seems a natural fit because estrogen and some of its metabolites have been shown in many systems to be a free-radical scavenger. Dr. Brann's preliminary studies support this, showing dramatically reduced levels of toxic superoxide, the major free radical, in stroke models treated with estrogen and tamoxifen before stroke. "We know they can do good things in other parts of the body, so what can they do to the brain?"

One additional good thing these substances may do is encourage stem cells found in the brain to rally to the stroke scene. "The old thought was that the number of neurons you have after development is all that you will ever have. The new thought is that is not exactly true," says Dr. Brann.

In fact, research has shown at least two areas of the brain have a nearby supply of stem cells that can develop into neurons and other types of brain cells.

Again, his preliminary work has shown that estrogen enhances this natural replacement process. "We can say the estrogen-treated group has more proliferation, neurogenesis is the word we use, going on in the subventricular zone of the brain four days after stroke."

Low and higher estrogen doses seem to work equally well; the jury is still out on whether tamoxifen and raloxifen can do the same. Dr. Brann is still looking at their impact and looking further at estrogen, too.

"Now what we have to do is look at two weeks, three weeks, six months. What happens? Do these new cells migrate out? Do they reach the area of infarct? We have to trace them. We have to track them. That is what the grant is about."


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Contact: Toni Baker
tbaker@mcg.edu
706-721-4421
Medical College of Georgia
12-Jul-2005


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