There have been a number of drugs which have been shown to slow beta-amyloid plaque development, but this is the first to show any reduction in cognitive decline in association with it. For instance, the same companies who development lecanemab also trialed aduhelm, which reduced plaques with no change in patient cognitive abilities. This was approved by the FDA as well with much controversy, resulting in the resignation of 3 members of the advisory committee. However, the results are modest with some scientists claiming it will not result in any perceivable difference for the patient. Indeed the above poster is correct in that there is a growing concern whether beta-amyloid plaques are the cause of the disease, as the foundation of the hypothesis has been called into suspect due to potentially fraudulent work. There was an interesting write up recently in Science about it. Now, this is not my field, but I'm curious of what may come out of it. It may be akin to a sort of Piero Anversa c-kit stemcell fall out, resulting in the retraction of a slew of studies.

But there is no breakthrough. This drug, like Aduhelm which is already out, does not slow not stop Alzheimer's disease. All people who get the treatment still progress in the same degree as withoit treatment. This drug is the same kind of treatment that Aduhelm is, which is a monoclonal antibody for plaques. Your statement that there are 0 drugs targeting amyloid is incorrect, as Aduhelm is already out for the public.

95% of all AD cases are sporadic with no genetic cause, the other 5% are from familial AD. These antibody drugs fail to do anything for sporadic cases and the only people there is any difference is with the 5% familial group. And that treatment difference disappears after a few months with the disease progress continues. The drug causes brain bleeds in more people than it does treating Alzheimer's.