'It confirms a new era of disease modification for Alzheimer's disease, an era that comes after more than 20 years of hard work by many, many people, with many disappointments along the way.'
Critically, the drug removed so much of the amyloid protein that the patients wouldn't have had enough evidence of Alzheimer's disease on their brain scans to actually qualify for entry to the trial.The study strongly suggests that the drug only starts to have a clinical effect once amyloid is reduced to low levels in the brain.
Lecanemab is not a cure. But even slowing the progression of Alzheimer's disease would be game changing, delaying the need for specialist care and allowing people to spend more time with their families.One in eight patients given lecanemab suffered brain swelling and other changes, probably as a result of removing the amyloid protein. But most only had evidence of problems on brain scans. Fewer than one in 30 had actual symptoms such as headaches or confusion.
Most Alzheimer's patients are currently diagnosed when they have moderate symptoms - too late for treatment with lecanemab. And just 1% have their diagnosis confirmed by a brain scan or lumbar puncture, a biopsy of their spinal fluid. "We estimate that unless there are drastic changes in how people access specialist diagnostic tests for Alzheimer's disease, only 2% of people eligible for drugs like lecanemab will be able to access them."
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