Leqembi is designed to target other forms of amyloid, though it also removes plaques. And the results with donanemab and leqembi are unlikely to end that debate.ĭonanemab is designed to target plaques specifically. "There's been a debate in our field for 30 years now about whether the plaques themselves are causing the problem," Sperling says. Eventually, these clumps end up in plaques between brain cells. But scientists have learned that when these molecules begin to clump together, they can take on forms that are toxic. Single amyloid molecules appear to be harmless. "We've learned to be more aggressive with dosing," she says, which quickly reduces amyloid to very low levels in the brain.īut scientists still aren't sure which forms of amyloid offer the best target. Instead of treating patients who've already sustained significant brain damage from Alzheimer's, researchers have focused on people whose brains are still relatively healthy.Īnother factor is the way researchers are approaching treatment, Sperling says. One reason for the recent success is earlier treatment, Sperling says. That approach, known as the amyloid hypothesis, had been in doubt after dozens of other amyloid drugs failed to help patients. The results with both donanemab and Leqembi provide strong evidence that removing amyloid from the brain can slow down Alzheimer's. About 6% had symptoms, like headache, nausea, and confusion. In the donanemab study, brain scans revealed this side effect in about 25% of patients. "I imagine in the future we'll have this initiation phase where we knock down plaque and then we'll have maintenance therapy," Sperling says.īoth donanemab and Leqembi can cause dangerous swelling or bleeding in the brain. But it's still not clear whether donanemab's benefits will persist for years after treatment ends. That appears to give donanemab an edge over Leqembi, which requires ongoing treatment. The plaques did not reappear during the 18-month study, and the benefit to memory and thinking continued. Patients were taken off the drug once the plaques in their brains were mostly gone, usually within a year. The study also suggests that patients may not need monthly intravenous infusions of donanemab for life. "What we saw is that the ability to slow disease progression is strongest if you catch this disease earlier," Skrovonsky says. They had only mild cognitive symptoms.Įven within that group, though, people with more advanced disease saw less benefit from the drug. The donanemab study focused on people whose brain scans showed plaques and other changes associated with early Alzheimer's. Beta-amyloid tends to form sticky plaques in the brains of people with Alzheimer's. "But we have to do better."ĭonanemab, like Leqembi, is a monoclonal antibody designed to remove a substance called beta-amyloid from the brain. Reisa Sperling, who directs the Center for Alzheimer Research and Treatment at Brigham and Women's Hospital in Boston. "I do think that will make a difference to people," says Dr. The company has submitted the results to the Food and Drug Administration and expects a decision by the end of the year.īut experts caution that donanemab is no cure, and that its benefit amounts to only about a seven-month delay in the loss of memory and thinking. Daniel Skrovonsky, director of research and development at Eli Lilly, which makes donanemab. "This is the biggest effect that's ever been seen in an Alzheimer's trial for a disease-modifying drug," says Dr. The result, published simultaneously in the journal JAMA, suggests that donanemab is at least as effective as the newly approved drug Leqembi (lecanemab), which was found to reduce progression by about 27%. In a study of more than 1,700 people, the experimental drug donanemab slowed the progression of Alzheimer's by about 35%, scientists reported at the Alzheimer's Association International Conference in Amsterdam. Patients in the early stages of Alzheimer's may soon have a new option to stave off the loss of memory and thinking.
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