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thestar.com
Kenneth Kidd
Feature Writer
DALLAS—Until the 1960s, the received wisdom was that once you became an adult, you had your full complement of brain cells. Hence your mother's stern warnings about protecting the only brain cells you'd ever have.
We've since learned that all mammals, including humans, give birth to new brain cells throughout their lifespan. But not all of those cells survive to become fully fledged neurons.
Somewhere along their journey to getting wired into the brain, they essentially commit suicide, a process called apoptosis, or programmed cell death.
For the most part, this is just the natural state of affairs. Biology isn't always efficient, discarding much of what it builds. Human embryos, for instance, wouldn't develop fingers if the cells between their digits didn't go through apoptosis.
The trouble is, as we age, the rate of programmed cell death in the brain increases. More and more of those new cells simply don't make it through the 30-day process of becoming fully connected neurons.
In effect, our brains lose some of their ability to repair themselves.
This, however, wasn't what Pieper was seeing in Room K3.406.
The relative multitude of new neurons that he eventually detected were the product of mice whose brains had been treated with a chemical compound dubbed P7C3 or, in subsequent tests, a derivative of P7C3 that proved even more effective.
The drug wasn't making the mice produce more cells, but it was somehow protecting more of those cells from apoptosis.
“Instead of 70 or 80 per cent dying along the route, only 40 or 50 per cent are dying,” says Steven McKnight, another University of Texas biochemist who worked on the study, published last month in the journal Cell.
This could have profound implications in treating what for many is the most terrifying brain disease associated with old age: Alzheimer's.
And if there's a research community that could...more next time on dementia views about The life of the brain: The promise of restoration
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