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 lifespan.

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.

Tachykinins, he added, "could then be the basis of future treatments."

The findings were reported in last week's issue of the journal Science.