Baker cautions that he has no idea if the same approach would work in other strains of lab mice that imitate the symptoms of Alzheimer’s in different ways—and much less if it would work in people. Alzheimer’s researchers have an atrocious track record of translating promising findings from rodent studies into actual treatments. After decades of false starts and failed clinical trials, they are understandably wary.

Nevertheless, most of these previous trials involved drugs that were designed to get rid of a different protein that’s thought to lie at the heart of Alzheimer’s, amyloid-beta. The concept of going after senescent cells is new. “If these cells are found to play important roles in people with neurodegenerative disease, the implications for treatment could be quite significant,” says Li-Huei Tsai from MIT, who was not part of the new study.

That’s because there are several “senolytic” drugs that can eliminate senescent cells, and some of these have already been approved for treating cancers. “If they prove effective in preventing or slowing neurodegeneration, it would represent a truly major advance, especially in light of the continued failures of amyloid-based clinical trials,” Tsai says.

Most people think Alzheimer’s is a normal part of aging.

Despite those failures, or perhaps because of them, the National Institutes of Health has dramatically increased its spending on Alzheimer’s research, tripling its annual budget over the past three years to $ 1.9 billion. This financial explosion was partly meant to entice new researchers into tackling the puzzle of Alzheimer’s—and in Baker’s case, it certainly worked.

His team, including Tyler Bussian and Asef Aziz, worked with a strain of mice that accumulates tau tangles in its neurons by six months of age. By eight months, the mice’s neurons have started dying, their brain has started shrinking, and their memories have begun to falter. But Bussian and Aziz found that all of these problems are preceded by the buildup of senescent cells, and can be prevented by eliminating those cells at an early stage.

They did this in two ways: first, by genetically engineering the mice’s bodies to destroy their own senescent cells when they are fed a particular chemical; and second, by using a senolytic drug called “navitoclax” that kills those cells directly. Both approaches were successful at preventing tau tangles.

Navitoclax was originally developed as an anticancer drug, and it’s one of several tumor-fighting drugs that might also double as a senolytic. To kill tumors, such drugs must be delivered at high doses, so that no tumor cells escape. But when killing senescent cells, total annihilation isn’t necessary, and it might be possible to get away with far lower doses. A company called Unity Biotechnology is busy developing several senolytic drugs, and Baker is an inventor on some of its patent applications.