Professor Matthew Kiernan

Right.

And the other thing is, we've obviously mentioned amyloid and tau and they're important parts, but they're not the whole story either.

Yeah.

And so there's a discussion.

I remember when people were talking about amyloid, they said, well, it's like saying if you remove smoke, is that the end of the fire?

No way.

So there's a whole process going on here.

And amyloid and tau are critical parts and the genes modifying them are critical parts.

But if we remove all of the amyloid out of someone's brain, will they be back to normal?

Well, no, they're not because we're doing that now.

So we can remove the amyloid with the monoclonal antibodies and

And they don't go back to normal.

They might either plateau or they might slow down the progression.

But then the question is, can we fine-tune that?

When do we start it?

Do we start these medications at the age of 30 when we see EPOE4 is up and monitoring some other parts of the biomarkers?

And that's where we're going.

We're going to go earlier and earlier and earlier.

And it might be that one of the medications is related to a gene modification in amyloid

in a few years' time.