Science & technology | Treating dementia

A drug for Alzheimer’s disease that seems to work

It is not perfect. And it has side-effects. But it may be the real deal

Alzheimer's disease. Coloured single photon emission computed tomography (SPECT) scans of axial (horizontal) sections through a normal brain (top) and that of a patient with Alzheimer's disease (bottom). The colours show different levels of activity within the brain tissue, with red showing high activity and black very low activity. The Alzheimer's brain is less active. Alzheimer's is a degenerative brain disease and a common cause of dementia in the elderly. It causes memory loss, confusion and personality changes. Its causes are not known and there is no cure. SPECT scans use a gamma camera to detect radioactive traces, injected into the blood, that accumulate in areas of high metabolic activity.

Editor’s note: On January 6th America’s Food and Drug Administration approved lecanemab, to be marketed as Leqembi.

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.

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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 create 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 a number of 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.

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This article appeared in the Science & technology section of the print edition under the headline "Enter lecanemab"

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