When I started reading the article I thought the title was a bit click-baity for Science. But then I noticed that the theory it refers to was not the amyloid hypothesis itself, but the toxic oligomer hypothesis that emerged later. That theory is pretty much the main potential explanation on why every single drug targeting Aβ failed that still keeps Aβ fibrils relevant. It's a very convenient theory because it keeps the main original observations about the fibrils relevant while explaining why therapies that target them don't work.
One part that is really important that is mentioned in the middle of the article is that these systems are very difficult to handle, and it's almost impossible to make many of them nicely reproducible. Fibril and oligomer formation depends a lot on the environment and reacts to tiny differences.
I find this kind of fraud deeply frustrating, there is so much wasted effort in the wake of faked high-profile results.
One part that is really important that is mentioned in the middle of the article is that these systems are very difficult to handle, and it's almost impossible to make many of them nicely reproducible. Fibril and oligomer formation depends a lot on the environment and reacts to tiny differences.
I find this kind of fraud deeply frustrating, there is so much wasted effort in the wake of faked high-profile results.