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Blood Clotting Role Examined in Alzheimer's

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By AlzheimersSupport Staff • • June 7, 2000

Researchers at the University of Kentucky Chandler Medical Center have discovered a possible clue into the cause of Alzheimer’s disease.

Led by Steven Estus, PhD, and H. Michael Tucker, PhD scientists from the United Kingdom, the study examined the molecular system that regulates blood clotting.

Blood clots routinely form in blood vessels. It is crucial that these clots be destroyed before they cause heart attacks or strokes. This destruction is accomplished by activating the plasmin system, which regulates the process of blood clotting and also plays a role in cell migration.

One of the principal molecules involved in regulating blood clots is called tPA. The U.S. Food and Drug Administration has approved synthetic tPA for use in treating heart attacks or strokes within a few hours of the onset of symptoms. The drug dissolves the blood clot that is causing the heart attack or stroke.

The first step in destroying blood clots is the production of the proteins tPA and uPA in tissues near the blood clot. The study explored was whether plasmin, another molecule involved in regulating blood clots, destroys amyloid-beta, the protein known to be found in the brains of Alzheimer’s patients.

Study Results

The results of their study, published in The Journal of Neuroscience, led the researchers to believe that they “can suggest a model of the development of Alzheimer’s disease.” Understanding the disease’s development is crucial to finding treatments.

Specifically the study showed that certain proteins found in Alzheimer patients’ brains stimulates the production of both tPA and uPA. It also discovered that plasmin destroys non-aggregated and aggregated amyloid-beta proteins as well as it destroys fibrin, and that plasmin appears to have no direct toxic effects in the brain.

Also, previous research has shown that the amount of the protein PAI-1, which inhibits the activity of tPA, is increased in Alzheimer's disease and inflammation, a common symptom of Alzheimer's.

"With these results and previous research, we can suggest a model of the development of Alzheimer's disease. Specifically, inflammation increases the amount of tPA inhibitors, which prevents the destruction of amyloid-beta proteins by obstructing the action of tPA. The increased levels of amyloid-beta cause further inflammation that feeds the cycle again," Tucker said.
"The particularly exciting thing about these results is that they suggest that it may be possible to treat Alzheimer's disease by destroying amyloid-beta protein deposits with tPA that is modified to target brain tissue," Estus said.

Further research will explore the accuracy of this model and whether tPA can be modified effectively to target brain tissue.

The study was funded by American Health Assistance Foundation, a private foundation that supports Alzheimer's disease research.


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