IT IS EASY to be cynical about announcements of drugs that claim to slow the progress of Alzheimer’s disease, the most common form of dementia. Lecanemab, however, may be the real deal. Results of a clinical trial, conducted by its makers, Eisai, of Tokyo, and Biogen, of Cambridge, Massachusetts, have just been announced in the New England Journal of Medicine. After 18 months, it had slowed the progress of symptoms by a quarter.
The trial involved 1,795 participants who were, crucially, in the early stages of the illness. Half received the drug. The others, a placebo. It showed two things. One was that modest but measurable slowing of progression. The other was that an explanation of Alzheimer’s called the amyloid hypothesis seems correct.
Beta-amyloid is a protein which accumulates in plaques in the brains of those with Alzheimer’s. It, and a second protein, tau, are established signs of the illness. But whether either or both is a root cause of it has been much debated. The success of lecanemab, an antibody that attaches itself to beta-amyloid and then attracts immune-system cells which clear the protein away (and measurably did so in those receiving the drug), suggests beta-amyloid does indeed directly cause problems associated with dementia.
This is a small first step. Some experts question whether the test used to show an improvement in symptoms is clinically meaningful. And lecanemab induced nasty side-effects—notably swelling and bleeding of the brain—in some participants. Also, diagnosing dementia this early is hard. Beta-amyloid can be detected by positron-emission tomography, but that requires a piece of expensive equipment. Or a sample of cerebrospinal fluid can be taken, which is unpleasant, and not something that could easily be turned into a routine screening programme. It is, however, a proof of principle. Now that the antibody approach has been shown to work, it can be followed up with other, similar, antibodies. Hope for more good news soon.
