It's a noble image: brain cells valiantly fighting for their lives
after astroke has cut off their precious blood supply. But some
researchers now think that a more macabre process occurs when a brain
artery ruptures or becomes blocked--mass suicide.
Scientists call it "programmed cell death," or apoptosis, and it
happens all over your body. Cells in the skin, for example, do themselves
in as they approach the epidermal surface, where they replace dead cells
that have sloughed off.
But unlike skin cells, neurons can't replenish their numbers by
dividing. Why kill themselves, then, in the aftermath of a stroke?
Because a damaged cell runs the risk of mutating, suggests Matthew
Linnik, Ph.D. Such a cell could become cancerous or wreak havoc in other
ways.
"If something goes wrong in the brain, it is far better for the
organism if the cell commits suicide than for it to potentially mutate,"
says Linnik, a senior scientist at the Marion Merrell Dow Research
Institute.
By inserting a gene that prevents programmed cell death into a tiny
section of rat brains, Linnik and Howard Federoff, M.D., Ph.D., of Albert
Einstein College of Medicine, reduced neuronal suicide after a stroke.
The brain area they protected was barely larger than the period at the
end of this sentence, but the implications of preventing apoptosis are
tremendous, particularly if the process turns out to play a role in such
neurodegenerative conditions as Alzheimer's and Parkinson's
disease.
Ironically, programmed cell death also occurs where you might least
expect it: in the prenatal brain. The brain of a human fetus has twice as
many cells as that of an adult, but half of those cells are weeded out in
the womb. If a particular fetal brain cell isn't necessary for developing
neural pathways, its suicide genes kick in.
"That genetic program is still there for the rest of your life;
it's just inactive," explains Linnik. He speculates that the suicide
program somehow gets reactivated when stroke or degenerative diseases
occur.
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