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Transcript
Meet the Scientist
The Role of Platelets in Malaria
and Heart Attacks
If you’ve taken high school biology, you know that your body needs
platelets to stop bleeding at the site of a wound. University of Rochester
researcher Dr. Craig Morrell, however, sees these good guys of the
circulation system in a little different light.
“When a platelet gets activated, it forms a blood clot so you don’t bleed
to death,” he said. “It also secretes inflammatory molecules, to promote
an immune response and recruit white blood cells to fight infection.
When we look at things like cerebral malaria, platelets can do bad
things by promoting inflammation.”
Craig Morrell, D.V.M., Ph.D.
Associate Professor, Department
of Medicine, Aab Cardiovascular
Research Institute
Many patients with vascular issues take cumadin or other “blood
thinners” to limit the effects of platelets, but these medications require
weekly blood tests to keep the levels appropriate for the patient’s health.
Finding a lower-maintenance alternative would improve quality of life
for millions of patients.
Dr. Morrell and his lab team used mice to discover that platelets can
be both good and bad in fighting infections like malaria. “Immediately
after we infect the mice, the platelets get activated, which helps activate the acute phase response,” he said. “But
later, the platelets cause inflammation, which leads to lesions in the brain.”
Dr. Morrell’s lab includes a cardiology fellow who researches
platelet activity after heart attack, revealing some important
insights. “After a heart attack, platelets attract the white blood
cells, which actually drive that heart attack,” said Dr. Morrell.
“The goal is to find the sweet
spot where you’re slowing
down platelet activation but
not preventing it.”
Antiplatelet therapy can alleviate some of this, but how much is too much? “The goal is to find the sweet spot
where you’re slowing down platelet activation but not preventing it,” he explained. “If you can regulate the
platelets in certain situations, you can slow them down without totally preventing activation. We’re looking at
potential regulators.”