For several days after a patient suffers a stroke, brain cells are bombarded with molecular 'pro-death' signals carrying such bad news about the brain environment that the cells are tempted, even urged by other molecules, to commit suicide. Many do. It's the main reason why most strokes aren't limited to a tiny area of the brain but damage a larger region as well.
In a bid to persuade fickle brain cells to live, University of Rochester scientists have enlisted an unlikely ally: the herpes virus. In an article published August 15 in the Journal of Neuroscience, the team announces a series of experiments where it used the virus to modify brain cells from mice, making the cells more resistant to death after a stroke. Like psychologists talking a despondent man down from the ledge, scientists kept cells from preventing suicide by thwarting the molecular machinery normally involved in persuading cells to self-destruct in a process known as apoptosis.
Once the brain has been traumatized by the low oxygen levels, or hypoxia, that stroke causes by choking off the blood supply, it unleashes a flurry of molecular signals encouraging still-healthy cells to kill themselves, magnifying the effects of the initial attack. The widespread self-destruction takes places for days or even a week after the initial stroke. It's a big reason why strokes are the leading cause of long-term disability in the United States, where there are about 4 million stroke survivors, roughly the same number of people as have Alzheimer's disease.
"Stroke is all about how cells deal with hypoxia," says neuroscientist
Howard Federoff, M.D. Ph.D., who did the study with graduate student Marc
Halterman and dermatologist Craig Miller, M.D. Ph.D. "Do they adapt and survive,
or do they withdraw and commit suicide?" asks Federoff, who has developed a
highly advanced system for using the herpes virus -- long the bane of cold sore
sufferers everywhere -- to manipulat
Contact: Tom Rickey
University of Rochester