How to pronounce “amylo” in English

Amyloid does not show up in the right places in the brain.

Amyloid, as I mentioned earlier, accumulates in the heart and it also accumulates in the brain during Alzheimer's.

The amyloid hypothesis postulates that A beta is front and center.

develop amyloid plaques in their brain and they get demented.

The amyloid protein, we really-- again, after decades of research-- really don't understand what it does normally, if anything.

And amyloid is actually the substance that accumulates in the brains of Alzheimer's patients.

So things like amyloid protein, for instance, which is associated with Alzheimer's risk, is being flushed out of the brain during sleep.

They're called amyloplasts. I won't go into the detail, but essentially, you can zero in on particular organelles that are very sensitive, a little bit similar to the way

that beta amyloid accumulation is the primary cause of Alzheimer's disease.

Guess where the amyloid precursor protein gene lives.

That accumulation of amyloid beta starts when we're healthy and probably reaches a near maximal level by the time patients--

do something to this amyloid protein to neutralize it.

They had amyloid vaccines ready to give to humans.

Not true of amyloid.

And that beta amyloid is something that, it also reduces neurogenesis.

Then there's amyloidosis, which actually has been discovered quite recently to be a major killer of the really elderly.

It's not just amyloid accumulating.

happens where some of the amyloid plaque that builds up in the brain that can tangle and get entangled with our neurons,

That's supportive evidence that amyloid is bad for you.

It can withstand a lot of amyloid plaques and a lot of tau tangles before a patient exhibits the first symptom.

We need to develop drugs against this amyloid protein.

It presumably helped to clear amyloid plaques out of the brain, but it was a little bit frustrating that it didn't seem to have any effect on the clinical course

They required people to have amyloid PET imaging in order to get into the trial.

It seems to be downstream of beta amyloid.

that have come from beta amyloid trials.

down to this thing called amyloid.

Extracellular junk-- this is stuff like the amyloid that form plaques in Alzheimer's disease.

and compare them using PET to look at amyloid and MRI to look at hippocampal volume and looking at cognitive function testing and biomarkers

And we came to understand that some cleavage event-- so that amyloid precursor protein gets cut at two different places in order

mediates one of those cleavage events in the amyloid precursor protein to liberate A beta.

And so scientists really got excited about this amyloid hypothesis.

So again, amyloid hypothesis-- here we are now, in the 1990s and everybody in the scientific field is super excited about the amyloid hypothesis.

So they had to demonstrate positive evidence that they actually had amyloid in their brain-- in other words, that they truly had Alzheimer's disease.

so about one year-- produce reductions in how much amyloid is in the brain, measured by that amyloid PET imaging.

And given the number of failures of drugs that target beta amyloid, a number of us are wondering, is the amyloid hypothesis dead?

Now, beta amyloid plaque is what accumulates in Alzheimer's.

Molecular garbage outside the cell-- there's something called senile cardiac amyloidosis which is now known to be the number one killer of people

You can have gum all over your brain, amyloid proteins in your brain, and be clear-minded.

And the discovery of all these pathways ended up leading to the postulation of the amyloid hypothesis, which is this statement--

But this great technology came into widespread use-- the use of an amyloid PET tracer.

So you put people into the scanner at baseline to make sure they have amyloid in the brain.

those extra insulin parking passes prevent your brain from getting rid of a chemical called amyloid.

And cognitive reserve, then when beta amyloid, if it does begin to accumulate, you are protected from it, for a very, very long time.

One of the sticky toxic proteins that it washes away at night is a protein called beta amyloid.

These plaques are made up of a protein that we came to discover called the beta-amyloid protein.

of-- this was when this A beta protein, this amyloid protein, was discovered as the main ingredient in these amyloid plaques.

We understood that this A beta protein was actually a subcomponent of a larger protein that came to be called amyloid precursor protein--

And they saw that there was actually a really tight association between that finding and the degree of amyloid plaques

So this is a technology where you can use a small molecule that binds with high affinity to amyloid plaques.