This is still preliminary work, but it heralds a completely new approach to dealing with Alzheimer’s—changing neural activity, rather than delivering drugs or chemicals. “It’s so different from what people have tried, but we are very excited about the possibility of bringing this to human testing,” says Li-Huei Tsai, an MIT researcher who led the study.

“It’s potentially transformative,” and not because of its medical implications, says Vikaas Sohal, from the University of California, San Francisco, who was not involved in the study. “Many neuroscientists, including myself, have traditionally thought about gamma oscillations as having a role in how neurons communicate and process information. We haven't really thought about how they could change the biology of cells. Put it another way: If gamma oscillations are part of the software of the brain, this study suggests that running the software can alter the hardware.”

Indeed, that software sometimes gets ignored. According to Tsai, scientists have made huge progress in understanding the genes and molecules that underlie Alzheimer’s. But there’s been relatively less work on how the disease affects the collective activity of neurons—or vice versa.

Her team began by letting mice run through a maze, and recording the brain waves in their hippocampus—a part of the brain that’s involved in navigation and memory. Typically, when the mice hit a dead end, you’d see a short, sharp burst of gamma waves. But when the team studied a breed of rodents that are especially prone to Alzheimer’s, they saw weaker gamma bursts, and less synchronicity between the firing neurons.

Earlier studies had found gamma disruptions in people and rodents with Alzheimer’s. But with one recent exception, these had always looked at individuals who were already in the late stages of the disease. By contrast, Tsai’s rodents had no large beta-amyloid plaques, and were totally asymptomatic. They were early in their disease, and yet they already had gamma problems. So what would happen, Tsai wondered, if they fixed those problems?

To find out, her team used a technique called optogenetics, in which neurons are loaded with light-sensitive proteins so that they can be activated by flashes of light. By sending 40 such flashes a second, the team could create gamma waves in the brains of their mice. And after doing so for an hour, they found that they had roughly halved the levels of beta-amyloid. “We were very, very surprised,” says Tsai.

The team showed that they had mobilized a class of janitorial cells called microglia. These patrol the brain, cleaning up dead cells and harmful proteins. After the gamma burst, the microglia doubled in both number and size, and started swallowing any beta-amyloid that was lying around.

It’s likely that gamma waves have other benefits beyond clearing beta-amyloid. For example, Jorge Palop, from the Gladstone Institute of Neurological Disease, has shown that enhancing these waves can improve the memories of mice with Alzheimer’s. And Sohal has found that the waves can lead to “profound and long-lasting improvements in learning.”