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New Add-on Treatment Can be Effective in Stroke

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Article 13

The protocol for care in the treatment of strokes caused by blood clots entails the therapeutic infusion of tissue plasminogen activator (tPA), which will dissolve the clots and repair blood flow within blood vessels. This “thrombolytic” remedy carries the hazard of bleeding and swelling within the brain, and it has to be administered within three hours after the start of the stroke, which sharply limits its clinical benefits.

Working with animals, researchers at Joslin Diabetes Center now have demonstrated the benefits of giving a drug in combination with tPA that could enhance stroke treatment effects and develop the window of opportunity for the treatment.

Medications that target a protein referred to as plasma kallikrein, as well as an activator protein referred to as factor XII,  may provide the opportunity to make tPA safer by reducing these issues and growing its efficacy in opening blood vessels, according to the authors of the study.


About 800,000 persons in the USA have a stroke each year, and about 87% are ischemic strokes, wherein blood flow is blocked through a clot.

The researchers were able to test that tPA boosts the function of plasma kallikrein in human and mouse plasma. They subsequent experimented with mouse models wherein blood clots had been prompted in the brain after which they were handled with tPA. Animals that had also given a plasma kallikrein inhibitor, and animals that have been genetically modified to supply reduced quantities of the protein, showed significantly less bleeding, brain swelling and brain damage than control animals without plasma kallikrein blockade.

The researchers traced the biological mechanisms by which tPA prompts plasma kallikren, via the factor XII protein, which promotes coagulation. Plasma kallikrein is known to set off the kallikrein kinin system, a pathway that has been implicated in stroke complications together with brain swelling and breakdown of the blood-mind barrier.

The FDA has approved a plasma kallikrein inhibitor for the remedy of hereditary angioedema. More inhibitors targeting this pathway are under development by many pharmaceutical organizations for this genetic disorder and other stipulations, together with diabetic macular edema. These new findings propose additional potential therapeutic possibilities for plasma kallikrein inhibitors in thrombolytic treatment.