There was absolutely no theoretical reason that some moldy cheese would kill bacteria but thankfully Fleming noticed what happened and we got antibiotics. Agai

There was absolutely no theoretical reason that some moldy cheese would kill bacteria but thankfully Fleming noticed what happened and we got antibiotics. Again, I'm in favor of people investigating all sorts of random shit. I agree that sometimes unexpected things pan out. If you want to run a carefully conducted, large long-term trial on ketogenic diets in Alzheimer's, I support you. I'm just skeptical it'll pan out, and on priors I'll put greater expectation on the approach with a scientifically demonstrated mechanistic theory behind it. I'm all for basic science when the statistical significance becomes so great it really starts to look like causality and then you start figuring stuff out. It doesn't seem like the statistical significance of the amyloid theory is strong enough that the direction of the arrow of causality can be determined. What are you basing this one? The p-value on lecanemab's single phase 3 trial was below 0.0001. And the causal role (not mere association) of amyloid in the disease has been demonstrated for years before significant efforts were invested developing therapies to target amyloid in the first place; most convincingly in the genetic mutations in APP, PSEN1, and PSEN2.