We've cured "Alzheimer's in mice" over and over again. Sadly our mouse model for Alzheimer's has not proven to be a good model for Alzheimer's in humans.
The only intervention I know of that shows robust results preventing Alzheimers is having been recently vaccinated. It doesn't seem to matter much for what, but several population studies, involving tens of thousands of patients and controlling for lifestyle confounders, show a reliable 40% reduction in dementia risk for people recently vaccinated for TDaP. Nobody will talk about it, apparently because it is embarrassing to have no clue why it works. (Pressed, people mumble about inflammation.) And, of course, no money is spent figuring it out, or figuring out why vaccination doesn't seem to help the other 60%.
Work in other countries has implicated herpes virus, and got good outcomes from valacyclovir, again provoking little interest from US researchers.
Whenever it, somehow, becomes possible to divert those two billion dollars to somewhere they might do some good for Alzheimer's patients, a whole population of biochemists who only know about brain metabolism in that mouse will need to find something else to do. In the meantime, they get to allocate the money to themselves.
Source? This sounds like a theory I would've seen here before.
https://www.sciencedaily.com/releases/2022/06/220624123814.h...
> People who received at least one influenza vaccine were 40% less likely than their non-vaccinated peers to develop Alzheimer's disease over the course of four years, according to a new study from UTHealth Houston.
This one tracked people vaccinated against flu every year, instead of (just?) TDaP. People vaccinated every year did better than those vaccinated fewer years, with the same 40% effect size. I wonder how many million people they will need to demonstrate the effect in, before any of the the mouse beta-amylase grant money gets diverted to figuring out how vaccines forestall it, and how many before any GPs start applying the (embarrassing) results.
Sci-hub doesn't have the paper, but it seems to be open-access: https://content.iospress.com/download/journal-of-alzheimers-...
Even if the animal model they tested it using is suspect, the theory behind drug itself (targeting senescent cells) is plausible.
I wouldn't give it more than a 10% chance but without other effective alzheimer's drugs even a small chance like that is absolutely still worth doing clinical trials on.