Max Lugavere

So

You know, back in the day when Alzheimer's disease was first named in 1906 by physician Alois Alzheimer, we had the tools of medicine were very rudimentary.

The only way to like actually diagnose Alzheimer's disease would be to open up the brain of a person who had died, the brain of a cadaver, somebody who died of Alzheimer's disease.

And you would see like plaque on teeth, you know, plaques in the brains of these, yeah, of patients who had died from the condition.

And that would be the gold standard way of diagnosing officially the cause of death being Alzheimer's disease.

But now we have, you know, I mean, now we can get way ahead of that with imaging, with functional imaging and stuff.

Um, and even metabolic indicators and, and blood biomarkers, like we're now starting to, you know, correlate levels of amyloid in the blood to, um, amyloid in the brain.

So it's there, it's definitely involved and especially late in the game, um, in, in Alzheimer's disease.

I mean, it does start to build and strangle neurons essentially because it builds up in the space around neurons and neurons are, you know, I mean, there are brain cells that are like, how are,

You know, they make up the networks of, you know, cellular machinery that are responsible for our thinking and feeling and like everything that it makes means to be human, right?

But what's actually causing it to aggregate in the brain?

That is the looming question.

And so...

Yeah, I think that the way that the field is turning, it's no longer looking at amyloid as being causal.

We're trying to get ahead of that.

And I think we're succeeding in many ways.

I mean, it could have something to do with insulin sensitivity in the body.

We know that insulin resistance in the body is strongly inversely correlated to glucose metabolism in the brain.

So you want to make sure that you're insulin sensitive.

You want to