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This month, the Food and Drug Administration approved a new drug, lecanemab, for the treatment of Alzheimer's disease. The drug, sold under the brand name Leqembi, was developed by Japanese pharmaceutical company Eisai and will be marketed commercially in partnership with American pharmaceutical company Biogen. Biogen, notably, is the maker of the drug Aduhelm, whose earlier rollout and marketing were a fiasco from scientific and public relations perspectives. Lecanemab is a humanized monoclonal antibody that binds to and lowers brain levels of amyloid beta, the protein suspected of contributing to Alzheimer's.
Results published Jan. 5 in the New England Journal of Medicine (NEJM) came from a multicenter study that enrolled 1,795 participants diagnosed with mild Alzheimer's. While the disease progressed in both groups, research subjects who were randomized to the lecanemab group showed slower progression of the disease when compared with subjects in the placebo group. Brain scans showed a significant lowering of amyloid in the lecanemab group when compared with the placebo group. Brain swelling and hemorrhage were greater in the active drug group when compared with the placebo group.
There was jubilation among members of the press. Based on the data, it was argued that the disease progressed 27% slower in the active treatment group when compared with the placebo group. The study was hailed as "momentous and historic" by the United Kingdom newspaper The Times.
This is the first amyloid-lowering drug that slows disease progression when compared with a placebo. The exuberance is understandable. However, we need to take a clear-eyed look at the data beyond the headlines. A thoughtful editorial published Dec. 3 in the prestigious medical journal The Lancet, "Lecanemab for Alzheimer's disease: Tempering hype and hope," argues that the 27% difference in disease progression between the drug and placebo groups translates to a much smaller objective difference in cognitive decline, estimated using the Clinical Dementia Rating sum of boxes (CDR SB) scale that quantifies a range of cognitive and functional domains. The difference between the two groups is 0.45 on the 0 to 18 scale, a difference so subtle that patients who receive the drug and their family members who care for them will not be able to notice the clinical difference. In other words, the difference is statistically significant but not necessarily clinically meaningful.
In addition, the side effects are potentially serious and will require close medical monitoring. The cost of this biweekly intravenous drug is estimated to be $26,500 per year.
On Nov. 3, 1906, German psychiatrist Alois Alzheimer presented the clinical features of Auguste Deter — the first patient diagnosed with the disease — together with the neuropathological features that included brain shrinkage and the presence of a protein found between brain cells (amyloid plaques) and the Tau protein identified within the brain cell.