Dominic D'Agostino

There's been not a whole lot of movement there.

We have the antibodies.

You go to antibody therapy, you're talking 50K at least, hundreds of thousands of dollars.

You have the potential for side effects like cerebral hemorrhage.

And they move the needle maybe for prevention.

A hallmark characteristic of Alzheimer's disease is glucose hypometabolism.

So that is actually being part of the criteria for evaluating.

My thoughts are that in communicating with hundreds of people with Alzheimer's and communicating with people that do dietary therapies is that there is a subset of people with Alzheimer's disease or let's just call it dementia because Alzheimer's is still a pretty fuzzy diagnosis.

Clinically, we have the PET scans to look at amyloid and then there's PTAL and other things.

I think it's better to put it under the umbrella of

mild cognitive impairment, I think it's important to focus on that and advance Alzheimer's disease.

A ubiquitous characteristic is glucose hypometabolism.

I've always been under the impression that the accumulation of amyloid and tau are a consequence, are downstream epiphenomenon of inflammation, neuroinflammation,

There's, of course, huge, I think there's like 50 different genes that can cause Alzheimer's disease.

So if we're talking about ApoE4 carrier, that's like, I don't know, 80% likely to get advanced Alzheimer's or early onset.

Yeah, if you have like two copies or even one copy.

Yeah, maybe even a bit less than that.

If you have two copies, you are destined to have it.

If you do nothing.

Yeah.