Max Lugavere

They don't meaningfully improve cognitive function.

And so there's been a growing chorus of voices in the field of neurology that have been suggesting all along that amyloid is there at the scene of the crime, but it's not causal with regards to the condition.

That it's a lagging feature of amyloid.

the pathophysiology of the condition, that there are other factors, there are other, you know, whether it's risk factors, other mechanisms that are driving cognitive decline and ultimately Alzheimer's disease.

And amyloid basically just shows up late.

And so one of the prevailing hypotheses as to what causes Alzheimer's disease is actually

has nothing to do with amyloid, but it's a reduced ability for the brain to create energy.

And this is known as hypometabolism.

So basically like a reduced ability of the brain's metabolic processes that create energy.

The brain is a very metabolically hungry organ.

It's responsible for 25% of your basal metabolic rate.

despite making up only two to 3% of your body's mass.

So it's a massively energy hungry organ.

In the brains of people with Alzheimer's disease, the ability to generate ATP from glucose is diminished by 50%.

And this begins long before the presence of amyloid.

And on top of that, I mean, again, all brains produce amyloid.

There doesn't seem to be a strong correlation between amyloid presence in the brain and cognitive function.

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.