He probably had familial Alzheimer's, which is genetic and can occur much younger. We understand fAD pretty well, although that doesn't mean we can doing anything.

This article is talking about sporadic AD, which is around 95pct of cases.

Is that really how the authors defined it? Hyperinsulinemia getting no love.

See my comment above, but you're thinking of GLUT4.

There have been several trials with metformin. Mixed results I believe, but there's certainly something there.

Ketogenic diet confuses me as well. I've always assumed that effect is mostly mediated by immune regulation, but I'm not sure.

It's more "type 3", since the diabetic types aren't stages. Also, patients can show brain insulin resistance without showing peripheral insulin resistance (diabetes). That's the crazy part.

This is an old and thoroughly disproven concept that wont seem to die. The brain is absolutely responsive to insulin. GLUT4 is highly expressed in some parts of the brain and requires insulin binding to translocate from storage vehicles to the plasma membrane. Hippocampal memory gets a lot of focus in this regard, which dovetails into Alzheimer's.

If you manage your insulin levels well, exercise, and keep a good diet then your risk levels will be about the same as the general population.

(This is pretty much my scientific wheelhouse)

45 is actually a decent N for a RCT with a within subjects design. The design increases statistical power significantly over a between subjects design, which is likely what you are picturing.