Reacción a "Reactions: data from Alzheimer's clinical trial with lecanemab antibody published"

The study is very robust. The essential data on efficacy, slowing disease progression by 27%, we already knew, but they gave secondary clinical and biomarker results and they are all very consistent and in the same direction. The safety data, despite some alarmist reports, also seem reasonable. The side effects are less than with aducanumab [an FDA-approved anti-amyloid antibody in the US]. Overall, I think they have cleared up a lot of doubts. 

The implications will be very important for the field, as it will probably be the first disease course-modifying treatment. The currently approved drugs are symptomatic, I don't think it's appropriate to compare them. At this conference, the idea that clinical response depends on whether you actually remove amyloid (Roche's ganterenumab removed much less than expected and it is thought that this may be the reason [for the failure of their clinical trial]; in a post-hoc analysis they found that those who had the most amyloid reduction got less worse) has gained a lot of traction. It will be very important to see the dose-response analyses on ganterenumab and lecanemab; and of course, donanemab [another anti-amyloid antibody developed by the Eli Lilly company] coming out in the spring. 

In terms of limitations, I don't see any relevant scientific limitations, the data are very solid. It is true that the efficacy is modest (27%) and that the consequences are dizzying. But the vademecum would be significantly slimmed down if the bar were set here, and I don't think the detractors are proposing to discriminate against Alzheimer's disease over other diseases.  

The only limitation, more political than scientific, is that the EMA (not the FDA) always asks for 2 trials. This is a giant one (1800 patients, compared to Roche's two trials of 900 each). I understand that Eisai/Biogen pre-agreed the trial conditions with the FDA and EMA, but we will see what happens in Europe.