PROTEIN DISCOVERY MAY LEAD TO ALZHEIMER'S TREATMENT

For the first time, scientists have succeeded in protecting animals from Alzheimer's-like brain damage, opening new doors to developing therapies against the devastating brain disorder in humans.

In rat experiments, Boston researchers said they have shown the accumulation of a common human brain protein, called amyloid B, causes nerve cell damage characteristic of Alzheimer's disase.Furthermore, Dr. Bruce Yanker of Boston's Children Hospital and his colleagues said they have been able to block amyloid B-related brain damage in rats by injecting them with another protein, a nerve protein called substance P.

Dr. Zaven Khachaturian, associate director for neurosciences at the National Institute on Aging, hailed the new work, published Wednesday in Proceedings of the National Academy of Sciences.

"Only in living animals can we evaluate the clinical effects of the beta amyloid protein. This research prevents Alzheimer's-like lesions in animals as we hope someday to do in humans," Khachaturian said.

Between 2 million and 4 million Americans suffer from Alzheimer's disease, a degenerative brain disorder that destroys mental abilities. The cause is unknown and there is no effective treatment.

Last month, two other teams of researchers reported they have bred genetically engineered mice that develop the amyloid B deposition found in human Alzheimer's disease patients. However, they did not report on ways to block amyloid B-related brain damage.

"Having ways to examine the causes of Alzheimer's disease and various methods of prevention in animals could save us years of research," said Dr. Gene Cohen, acting director of the National Institute on Aging.

While the exact role of the amyloid B protein in Alzheimer's disease remains unclear in humans, it tends to accumulate in the brains of people with the disorder.

Yanker's team produced rats with Alzheimer's-like brain cell death by injecting human amyloid B protein into the part of their brains responsible for learning and memory.

When given within 24 hours of amyloid B injection, substance P blocked brain cell death in the rats. However, the substance P could not guard against brain cell death when given three days after the amyloid B injection.