- [Voiceover] If we take
a look at the brain tissue that's been affected
by Alzheimer's Disease under a microscope, there's
almost always two common factors that we'll see, and these are
called plaques and tangles. Let's just look at these
plaques for a minute. Well, actually, they're
called beta-amyloid plaques. Amyloid is the name we use
for fragments of proteins, so it's like not the whole
protein, just little bits of it. And these are produced
normally in the body. Beta-amyloids are protein
fragments that have been snipped off of the larger
protein by specific enzymes. So, you have your neuron with this protein called amyloid precursor
protein sort of sticking out through the cell's membrane. And so, how beta-amyloid
forms is when these enzymes swing by and chop off our
beta-amyloid protein fragment. These little beta-amyloid
snippets are somewhat sticky, and they'll start to clump together. And as they clump, they
mix with other molecules and even other neurons, forming
what's eventually called beta-amyloid plaques. Now, it's thought that
these clumps of plaques, especially the smaller ones, may interfere with the cell-to-cell
communication between the neurons, essentially blocking the
signal at the synapse. It's also thought that they might activate the immune response as well,
which triggers inflammation and also tells your
immune cells to root out and destroy the disabled cells. Now, it's super, super important
to note that this process is still not very well understood. It's especially unclear
whether beta-amyloid plaques themselves contribute to
causing Alzheimer's Disease or if they're essentially just
a result of the progression of Alzheimer's Disease. So, those are the plaques. Now, let's talk about these tangles. Another more fancy name you might hear is neurofibrillary tangles. And these, unlike the
beta-amyloid plaques, actually show up inside the neurons. So, usually, healthy neurons
are internally supported by and partly made up of these structures called microtubules. These microtubules are like
tracks that guide nutrients and other molecules from
the cell's body down to the cell's axon, which
is usually connected to another neuron. And this is basically how the neighboring neurons communicate. So, you could think of these
microtubules like rails that carry a mining cart
with a bunch of sweet ores and minerals, which
are like the nutrients and the messages, to the other miners, which are like the other neurons. Now, a special protein simply called "tau" binds and stabilizes our rails. Kind of like how railroad
spikes keep our rails in place, these tau proteins keep
our microtubules in place. In Alzheimer's Disease,
these railroad spikes, the tau proteins, are chemically changed and basically aren't the
right type of spikes. And instead of holding
the tracks together, they pair with other tau proteins. And when they do that,
they get all tangled up with each other. And since the tracks don't
have anything holding them together anymore, what do they do? Well, they start to fall
apart, and so our microtubules fall apart, and these tau
proteins become tangled. And since our track is all
messed up, this disrupts our whole transport system. And when this happens, we call
them neurofibrillary tangles. Since the tangles are sort of
like these thread-like fibers or fibrils, we say "fibrillary." And since they're in
the brain, we say that they're "neurofibrillary." And it's thought that the
disruption of our rail system causes some communication
issues between our neurons. And since they can't communicate
or transport our materials, they eventually are
decomissioned and undergo nerve cell death. Now, these plaques and
tangles can be found in brains of many elder people, but
they're found to a much, much greater extent in the brains of those with Alzheimer's Disease. And for Alzheimer's, they
tend to start forming and spread from the cortex
in a pretty predictable way, as Alzheimer's progresses. The earliest areas affected
are usually those associated with learning and memory,
here in the temporal lobe. And as it spreads and
more neurons are affected, it usually goes up to the frontal lobe, where thinking and
planning become affected. And then, more of the temporal lobe, as speaking and communicating
become affected as well. And then, it kind of moves
up into your parietal lobe, where your sense of where your body is in relation to objects
around you becomes affected. In severe and late-stage
Alzheimer's Disease, these plaques and tangles
have spread throughout most of the cortex. And as this happens, the
cortex gets seriously, seriously damaged. And due to this widespread cell death, the brain actually shrinks dramatically. But since Alzheimer's
progresses at different rates for every patient, the rate
of spreading of these plaques and tangles varies a lot
from patient to patient.