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Researchers say they have hopeful news for people with Alzheimer's. They delivered that news at a meeting in Amsterdam. An experimental drug appears to be even better at slowing down the disease than another one that was just approved by the FDA. Here's NPR's Jon Hamilton.
JON HAMILTON, BYLINE: The news came at the Alzheimer's Association International Conference. It involved positive results from a large study of the drug donanemab. At a press briefing, the association's chief science officer, Maria Carrillo, offered this reaction.
MARIA CARRILLO: There is a palpable excitement about what's happening in our field. This decade is already proving to be the decade of Alzheimer's, and I think it will continue to increase and get better from here.
HAMILTON: Later, the drug's maker, Eli Lilly, provided detailed results of its study of more than 1,700 people. Dr. Daniel Skovronsky is Eli Lilly's head of research and development.
DANIEL SKOVRONSKY: This is the biggest effect that's ever been seen in an Alzheimer's trial for a disease-modifying drug, somewhere in the range of 35% slowing of disease progression.
HAMILTON: Another drug, called Leqembi, or lecanemab, had slowed the disease by about 27% in a different group of patients. Leqembi received full approval from the FDA early this month. Skovronsky says the new drug, donanemab, worked best in people just beginning to experience problems with memory and thinking.
SKOVRONSKY: What we saw is that the ability to slow disease progression was strongest if you catch this disease earlier.
HAMILTON: Donanemab clears sticky amyloid plaques from the brain, and in this study, patients stopped getting monthly infusions of the drug after brain scans showed the plaques were largely gone. Skovronsky says the idea was to find out whether patients would continue to benefit even after treatment ended.
SKOVRONSKY: And the answer was yes. So it's really exciting to think that this is a drug that can be used in many patients probably for a pretty limited duration, 12 months or less.
HAMILTON: Patients on Leqembi, the drug just approved by the FDA, must keep receiving infusions indefinitely. Both drugs can cause swelling or bleeding in the brain. In the donanemab study, brain scans revealed these side effects in about 1 in 4 patients. Skovronsky says a few of them also had symptoms like headache or confusion.
SKOVRONSKY: So 6% of people on the therapy - they have these imaging abnormalities and then symptoms which could be mild, but in a few patients, it was severe. And three patients who had these symptoms ultimately died.
HAMILTON: The results with both the donanemab and Leqembi provide strong evidence that removing amyloid from the brain can slow down Alzheimer's. The successes come after many other amyloid drugs failed to help patients. Dr. Reisa Sperling of Brigham and Women's Hospital in Boston says one reason the new drugs are working is that they are being started sooner, before the brain has been badly damaged.
REISA ANNE SPERLING: I also think we've learned to be more aggressive with dosing. And both these two trials really suggest you have to knock down that amyloid from baseline. You have to do it quickly.
HAMILTON: But it's still not clear which forms of amyloid drugs should target. Sperling says single amyloid molecules appear to be harmless, but when they start to clump together, they can take on forms that are toxic.
SPERLING: Eventually, lots of amyloid ends up in plaques in the brain. And there's been a debate in our field for 30 years now about whether the plaques themselves are causing the problem.
HAMILTON: Donanemab is designed to target plaques specifically. Leqembi, the approved drug, also goes after other forms of amyloid. Yet Sperling says both drugs appear to stave off cognitive decline in patients with early Alzheimer's.
SPERLING: This gives me hope that if you went even earlier, 10 years earlier, you could flatten the curve altogether one day.
HAMILTON: A big study to test that idea is already underway.
Jon Hamilton, NPR News. Transcript provided by NPR, Copyright NPR.
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