The most prevalent form of dementia, Alzheimer’s disease, has a reputation for progressing slowly, so news of new medications making this claim can be viewed with cynicism. But the real bargain might be Lecanemab. The New England Journal of Medicine has just published the findings of a clinical trial carried out by the product’s manufacturers, Eisai of Tokyo and Biogen of Cambridge, Massachusetts. It reduced the rate of symptom progression by around 25% over the course of 18 months.
1,795 patients who were still in the early stages of the illness participated in the trial. The medicine was given to half. Others are a placebo. This revealed two things. One was that slight but discernible slowing of growth. The other was that the amyloid hypothesis, a theory put forth to explain Alzheimer’s, appears to be accurate.
The protein beta-amyloid builds up in plaques in the brains of people with Alzheimer’s disease. It and another protein, tau, are recognised symptoms of the condition. However, it has been hotly contested as to which, if either, is the real origin of symptoms. The effectiveness of lecanemab, an antibody that binds to beta-amyloid and draws immune cells that eliminate the protein (and did so measurably in those taking the medication), suggests beta-amyloid does indeed directly cause issues related to dementia.
This is only the beginning, Lecanemab caused unpleasant side effects, particularly brain enlargement and haemorrhage, in a number of subjects. A dementia diagnosis at this stage is challenging. Positron-emission tomography is a method that can identify beta-amyloid symptoms. However, that calls for a costly piece of machinery. The alternative is to extract a sample of cerebrospinal fluid, which is uncomfortable and not something that could be simply added to a regular screening programme. But it serves as a principle-proving example. Since the antibody strategy has been proven effective, it can now be continued with additional antibodies and at advanced stages of the disease.