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Derek Lowe has seen it coming years ago https://www.science.org/content/blog-post/lecanemab-and-alzheimer-s-more-data

But let’s stipulate that the result is real, for the sake of argument. That takes us into the very contentious question of real-world utility. As the NEJM paper says, “A definition of clinically meaningful effects in the primary end point of the CDR-SB score has not been established”. Clinicians are already disagreeing over whether the difference between lecanemab and placebo is something that would even be noticeable. That last link features a quote of Madhav Thambisetty, a neurologist at the National Institute on Aging: “From the perspective of a physician caring for Alzheimer’s patients, the difference between lecanemab and placebo is well below what is considered to be a clinically meaningful treatment effect”. This is not an uncommon take.

And that leads to question 3. A constant problem with these anti-amyloid antibody ideas is the complication of brain edema, an inflammation response that can be serious trouble. The term of the art is “amyloid-related imaging abnormalities with edema or effusions”, ARIA-E. This latest trial kept a constant watch for this, as well it should have, and any such trial also has to keep in mind the possibility of “functional unblinding” as any incidents develop. ARIA-E was noted in 0.8% of the treatment group (and in none of the placebo patients, naturally). Overall, adverse events that were enough to lead to patient discontinuation in the trial occurred in 6.9% of the treatment group and 2.9% of the placebo group. Most seriously, two patients in the treatment group have died from what could well be treatment-related vascular issues

There was also earlier anti-amyloid antibody that got approved despite showing no benefit at all https://www.science.org/content/blog-post/they-don-t-know