Researchers have found an important clue to how a brain protein may produce Alzheimer's disease and how it may be possible someday to prevent the protein's toxic effects.
The protein, called amyloid-beta, is deposited in brain cells of patients with Alzheimer's disease.Studying its effect on rat brain cells growing in a laboratory, Bruce A. Yankner and colleagues at Harvard Medical School found that a piece of the protein stimulated growth of young brain cells but poisoned older ones - damaging their connections with other nerve cells and reducing their life span.
The toxic piece of amyloid-beta turned out to resemble a family of natural brain substances called tachykinins.
When the researchers added both amyloid-beta and tachykinins to dishes containing the older cells, they discovered that certain tachykinins completely prevented amyloid-beta from damaging the cells.
"If it can be shown that amyloid-beta is the critical factor in causing selective nerve cell loss, we will have a major handle on slowing or stopping Alzheimer's disease," noted Zaven Khachaturian of the National Institute on Aging, which helped fund the research.