Another new drug may temporarily halt the mental decline caused by Alzheimer’s disease, scientists say.
According to data presented July 17 at the Alzheimer’s Association International Conference in Amsterdam and published the same day in JAMA a drug called donanemab slowed cognitive decline by about 35 percent for one and a half years.
The discovery comes just weeks after the US Food and Drug Administration gave full approval to another drug called lecanemab (brand name Leqembi), which may also slow the progression of the disease. Another similar drug, known as aducanumab (Aduhelm), received accelerated approval last summer, although access to it is still very limited.
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These drugs target amyloid, a sticky protein that builds up in the brains of people with Alzheimer’s disease. The advent of this new treatment approach marks a turning point in what has been a long, arduous effort to find ways to slow down the disease.
“I think it’s a really big change,” says neuroscientist Jeffrey Cummings of the University of Nevada, Las Vegas. “This is one of the rare occasions when the word ‘breakthrough’ can be used.”
The developments may bring some hope to the 6.7 million people age 65 and older in the United States who have Alzheimer’s disease. Even so, many questions remain, including who should receive the drugs, how well they work, and how to weigh the potential benefits against the risks, which can be significant.
One thing is already clear: medicine is not for everyone. They are associated with risk and require careful monitoring. And, even if a person is a good candidate from a medical standpoint, the high cost, limited availability, and time-intensive dosing regimens can prevent widespread drug use.
Here’s what you need to know about these new drugs.
How do these Alzheimer’s drugs work?
The “mab” at the end of their unwieldy names—donanemab, lecanemab, and aducanumab—is the key to how they work: All three drugs are monoclonal antibodies.
These specially designed antibodies are inspired by antibodies that the body produces to detect harmful substances, a key part of the immune system. In the brain, lab-made antibodies attach to certain parts of the amyloid plaques that are characteristic of Alzheimer’s disease. When antibodies attach to amyloid, they trigger other immune cells to carry out the debris.
Recent clinical trials show that this cleansing work has mental benefits. And this discovery supports the idea that amyloid plaques are a key part of Alzheimer’s disease, an old idea called the “amyloid hypothesis.”
Failed clinical trials have forced some researchers to abandon the idea. “People were almost ready to give up on amyloid altogether,” says neurologist and neuroscientist Eric Musiek of Washington University in St. Louis. “I don’t think many people thought plaque removal was such a big deal.” But this new class of drugs suggests that plaques are not innocent bystanders.
Instead, the plaques actually seem to harm brain function, and getting rid of them helps, Musick says. “It seems to indicate that getting these plaques out of there is important.”
