Dominic D'Agostino

Your genes are not your desk.

I don't want to make that sort of assumption, but it puts you at greater risk for sure.

So just taking a step back, I think inflammation is the major driver.

And that wasn't even on my radar probably the last time we talked or maybe 10 years ago.

But I

I do think that systemic inflammation leads to neuroinflammation.

And we know that if we take mice and inject LPS, we can rapidly cause amyloid progression.

Those studies have been done.

So metabolic-based therapies, ketogenic therapies, diet, these things not only change metabolic physiology and brain energy metabolism, but they reduce systemic inflammation.

And I don't know if you measure your inflammatory markers like HSCRP,

Mine is even non-detectable.

I'll even do things like work out really hard.

It only was elevated when I lived in an undersea environment and was breathing hypercapnic under a lot of stress.

But I think the advantage of ketogenic metabolic therapies for Alzheimer's disease is really hinging upon suppressing inflammation, improving glucose metabolism, and elevating ketones to increase symptomatically brain energy metabolism.

You have the acute effects.

So I think what we can say that acutely, if we elevate ketones in the context of a cognitive deficit,

we can improve cognition under a battery of different exams.

But the question that investigators are after is that if you do an amyloid PET scan at baseline and two years, five years, 10 years, that is of the highest interest because amyloid is basically, that's the prerequisite for having Alzheimer's disease.

So those studies are ongoing and I'm connected with some investigators that are doing it and some that have done more acute studies.

And the feedback is that I think there's a subset of people, most people respond favorably, but there's also a subset of people that are hyper responders.