The finding, to be published Thursday in the journal Nature, reveals a new potential drug target that, according to the prevailing hypothesis of the genesis of Alzheimer’s, could slow or halt the devastating effects of this now untreatable disease.

The work involves laboratory experiments and studies with mice  it is far from ready for the doctor’s office. But researchers, still reeling from the announcement two weeks ago by Eli Lilly that its experimental drug turned out to make Alzheimer’s worse, not better, were encouraged.

“This really is a new approach,” said Dr. Paul Aisen, of the University of California, San Diego. “The work is very strong, and it is very convincing.” Dr. Aisen directs a program financed by the National Institute on Aging to conduct clinical trials of treatments for Alzheimer’s disease.

Over the past few years, research on Alzheimer’s has exploded. Now, Dr. Aisen said, about 200 papers on the subject are published each week. There are new scans and other tests, like spinal taps, to find signs of the disease early, enabling researchers to think of testing drugs before patients’ brains are so ravaged. And companies are testing about 100 experimental drugs that, they hope, will fundamentally alter the course of Alzheimer’s disease.

Most of the new drugs focus on an enzyme, gamma secretase, that snips a big protein to produce beta amyloid. The problem in Alzheimer’s is thought to be an overproduction of beta amyloid  the protein is made in healthy brains but, it is thought, in smaller quantities. Its normal role is not certain, but researchers recently found that beta amyloid can kill microbes, indicating that it might help fight infections.