That's a decent summary of the paper, though it's important to note that the "structure corrector" is, at this point, more of a "compound"--there's a lot more w

That's a decent summary of the paper, though it's important to note that the "structure corrector" is, at this point, more of a "compound"--there's a lot more work to be done before you'll be able to pick some up at CVS. I also want to quibble a bit with your "strength ranking": it dramatically understates the value of in vivo experiments in animal models. Animals do differ from humans in some known--and presumably other unknown--ways, and this has certainly caused issues in the past. For example, the subjects in the CB28-SuperMAB trial all became seriously ill despite successful tests in rabbits and monkeys. However, a major advantage of in vivo data is that it can give you a "whole organism" perspective on a possible treatment. This ensures that the therapy is targeting the actual condition (cognitive deficits) and not just a biomarker/side effect/epiphenomena. As an analogy, you want to actually fix a car's engine, instead of just turning the radio up until you can no longer hear the misfires. The Alzheimer's field has had issues with this before. ABeta is associated with Alzheimer's disease. While it's possible to reduce Abeta levels (e.g., with an antibody), this does not seem to have much effect on the mental symptoms.