Stroke is the third-leading cause of death in the United States and the number-one cause of severe neurological disability, accounting for about $75 billion per year in related costs.
Meanwhile, the closest we’ve got to an approved drug for stroke is actually a clot-buster that, if given very soon after the stroke, can at least dissolve the obstruction that’s cutting off the blood supply to the brain. But it doesn’t address the severe inflammatory damage that occurs after the stroke.
A new study led by Stanford’s Katrin Andreasson, MD, has identified a new target: a receptor found both on nerve cells and on endothelial cells that line the copious capillaries crisscrossing the brain. When stimulated, this receptor both strengthens nerve cells’ ability to survive after a stroke and causes blood vessels to dilate, allowing increased blood flow to both the damaged core area and the at-risk region around it.
I go into more detail in a release on the study. And I also describe how Andreasson’s findings may help explain why a much-heralded class of anti-inflammatory drugs that included the now-withdrawn Vioxx turned out to have some unanticipated cardio- and cerebrovascular side effects.