Breakthrough in Alzheimer’s Is Reported : Science: Salk researchers find a possible cause of cell death in the brain, and say Vitamin E may slow process.

Researchers at Salk Institute and UC San Diego announced Thursday that they have discovered one possible cause of the cell death that occurs in the brains of victims of Alzheimer’s disease.

The work of three researchers from the Salk Institute and one from UCSD also reveals that Vitamin E can inhibit the death of nerve cells caused by a protein that accumulates in the brains of those suffering from Alzheimer’s.

The research of David Schubert, Christian Behl and John Davis from the Salk Institute and Greg M. Cole from UCSD began with a study of the toxic effects of beta amyloid protein, which accumulates in clusters of dead brain cells called plaques.

Presence of such plaques is considered to be a distinguishing characteristic of the brains of Alzheimer’s patients.

“One of the critical clues as to what is going on, or what is going wrong, in Alzheimer’s disease, is these plaques,” said Kenneth Klivington, a spokesman for the Salk Institute. “There is a lot of debate in the scientific community about the root causes of Alzheimer’s.

“But people have known all along that these plaques show up in the brain. The key issue here is that there is no way of absolutely diagnosing Alzheimer’s, at the moment. The only way to know for sure is to autopsy the brain and look for these amyloid plaques.”

Klivington explained that plaques are a “key feature of the brains of Alzheimer’s patients, but whether they are the cause or consequence is up for grabs.”

But the principal chemical found in the plaques is toxic to the nerve cells of the brain, so, in his words, “it points the finger--there’s a smoking gun there in the amyloid plaques.”

What Schubert and his colleagues did, Klivington said, was demonstrate “clearly that the principal component (in the plaques) is toxic to nerve cells, and secondly, that Vitamin E can dramatically reduce the toxicity of this protein.”

“It suggests that one way of slowing down the damage done by Alzheimer’s is to provide a diet high in Vitamin E,” Klivington said. “And, perhaps, to take a supplement as well. In other words, it suggests a real way of going about things,” to slow the disease.

Although other scientists have found recently that plaque protein is toxic to nerve cells, Klivington said Schubert and his colleagues were the first to show that even low concentrations of the protein can kill other cells but are most toxic to nerve cells.

In experiments, the researchers applied Vitamin E along with the amyloid protein and found that most of the nerve cells survived. Vitamin E is an antioxidant known to prevent some types of cell death, but, the researchers say, this is the first demonstration of its ability to prevent cell death related to that in Alzheimer’s.

“We can’t make claims about the curative powers of Vitamin E,” Schubert, the chief researcher, said Thursday. “But it can prevent the killing of cells by this protein, and gave us a good way to study the actual mechanism of how nerve cells are killed.”

Still, Schubert recommends a diet rich in fruit, grains and vegetables supplemented with Vitamins E and C, as well as beta carotene as a possible way of postponing “some age-related damage to the brain.”

Schubert said “the next step” is to apply the research in clinical trials, though laboratory animals have not gotten Alzheimer’s, Klivington said.

“I’ve seen some reports that you can make mice get Alzheimer’s, but that’s not correct,” Schubert said. “There have been no good animal models for Alzheimer’s.”

But some research is being conducted to see what effect the beta amyloid protein has on animals’ nerve cells, and then what effect Vitamin E has on arresting any damage.

Cole, the UCSD researcher, said the next step for him will be to try “to understand how beta toxicity works at the molecular level, and to see if we can show protection against it in working with animal model”--in this case, by injecting the protein into the brains of rats.

“Previously, we’ve found we could see toxicity in rats by using a beta protein. Now, we’re trying to see if Vitamin E offers protection,” Cole said.

Cole said he was so sold on the virtues of Vitamin E that he is taking it himself, as are many of his colleagues.

“If beta protein toxicity plays a causal role (in Alzheimer’s disease), this is the first evidence that we have something that affects it or protects against it,” Cole said. “Administering Vitamin E is then perfectly feasible. . . .

“The real problem with Alzheimer’s is that it is strongly age-related. It occurs in less than 1% of the population under the age of 65, but recent evidence indicates that, in people between 85 and 90, the incidence is up to 47%.

“So, there’s a marked, exponential increase with age. What we hope to do is delay the disease enough that we can slow down its rate of progress so that we won’t be seeing it as much. That’s why we remain so interested in Vitamin E.”