Thank you for your comment and for pointing out that comparison. To be honest, I'm not so sure what to do with these physiological frenemies as well.

In part III, I discussed that the amyloid gene (i.e., amyloid precursor protein and its βA4 sequence) is important in cell adhesion and neuronal synaptic formation. So, attempts to develop a switch that could stop amyloid fibril formation would need to be careful not to impair other important biological functions.

One of the closest things we have to this switch is probably molecular tweezers, which can inhibit protein aggregation. While it works against AD in animal models, no published clinical trials have investigated it as far as I know.