Lecanemab slowed decline at an early stage, but it probably won’t benefit those with non-Alzheimer’s dementia, or those in the later stages of Alzheimer’s.
My father died last year from Alzheimer’s. As a son, I remember well the despair I felt as he declined. I was desperate for something — anything — that could help slow or reverse his decline. Judging from my experience, I think it is possible that patients and their caregivers will reach for lecanemab, an experimental drug for Alzheimer’s, like a lifeline.
Lecanemab, a monoclonal antibody administered intravenously every two weeks, targets and eliminates accumulations of beta amyloid, an abnormal protein widely believed to damage the brain in Alzheimer’s disease. The trial, published Tuesday in the, provides the first definitive evidence that removing beta amyloid in Alzheimer’s patients provides clinical benefit.
Given the cognitive benefits seen with lecanemab, the Food and Drug Administration is expected to grant “accelerated approval” to the drug in early January. This status would allow the drug to be given to patients in the general population but would possibly require Biogen and Eisai to conduct further trials of the drug to get full approval.The lecanemab results come after decades of failures in the field of Alzheimer’s research.
The FDA panel emphatically rejected this interpretation. That decision seemed to quash not only the hopes of treating the more thanin the United States — and about 30 million around the globe — living with Alzheimer’s but also in many ways the very rationale of the prevailing research program.
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