Translator: Claudia Sander Reviewer: Queenie Lee
I'm working on brain killers.
Brain killers?
Yes.
Alzheimer's, Parkinson's, Huntington's, prion diseases,
frontotemporal dementia.
They're also called age-related neurodegenerative diseases
because our chances to get one of these increases as we get older.
Ten percent of people aged 65 or more do have a neurodegenerative disease,
and there are no cures for them.
Current treatment, if available at all,
only alleviates symptoms and for a limited period of time.
30 million people in the world have Alzheimer's disease,
and about five times less have Parkinson's disease.
The number of people with Alzheimer's disease
will increase to about 100 million in 2050.
Why such a stunning increase?
Well, we get older,
and our life expectancies will continue to increase in coming years.
That's awesome, isn't it?
But the question we have to ask ourselves is,
"Does it make sense if we're not able to keep our brains working properly
during all these extra years?"
By the way, the cost of care for Alzheimer's disease patients
will become unaffordable.
From a cost of currently 200 billion dollars per year,
for the American society,
it will increase to 1.2 trillion in 2050.
We have to stop this new epidemic.
One of my best friends, Zack, told me his story.
He had an uncle called Bob.
He loved him.
Bob had been a nurse in a surgery department for all his life.
He never married.
He was always secretly in love
with one or another of his female colleagues in the department.
He was so smart.
He was the most resourceful person on Zack's planet.
He knew how to deal with injuries, those of the body and those of the mind.
But Uncle Bob's greatest attribute was his sense of humor.
By the way, he always knew how long it would take for a patient to recover.
He had his own criteria and he was rarely wrong.
Zack cherished to go for bicycle rides with his uncle.
Sometimes they would get lost.
So Uncle Bob would stop, sit up straight on his bicycle and emit a loud "Darn!",
which was the highlight of the ride.
(Laughter)
They would eventually find a way home,
it didn't matter how long it would take them.
After a long winter, where Zack had been very busy traveling,
Uncle Bob went for a bicycle ride on his own,
but this time he didn't return.
A good man found him sitting next to his bicycle
and brought him back.
This was the beginning of a long downhill road
from which there was no return.
Uncle Bob kept his humorous demeanor for quite a while,
letting go a "Darn!" when he didn't remember
what his nephew had told him one hour ago
or when he was unable to learn a new game.
He self-diagnosed with Alzheimer's disease,
but he didn't try to guess how long it would take him to recover.
Rightly so.
He progressively forgot everything,
from how to use the water faucet to who Zack was.
But what he kept for the longest
was his love for this man who pretended he was his nephew.
After six years,
Uncle Bob left for a place where bicycles are no longer needed.
I'm a scientist.
The reason why I'm talking to you today
is because something very important is changing.
15 years ago scientists were still arguing about which protein is responsible
for the mess in the brain of a person who has Alzheimer's disease.
But after years of lab work around the world,
of testing new hypotheses with newer methods,
of developing new experimental models,
the puzzle of the disease process finally assembles.
In our brains, we have cells called neurons.
Neurons are born to communicate,
so they have long extensions
that convey information from one neuron to another
by electrical and chemical signals.
They also have a cell body that contains their genetic code
and most of their little factories to produce energy and proteins.
Proteins are very important molecules in our bodies.
They have many functions,
such as maintaining a scaffold,
transporting one molecule from one place to another,
facilitating chemical reactions, or even cutting something.
They're then called enzymes.
Now I want to show you what's happening with one particular protein
which is present inside and at the surface of neurons.
Let's pretend for a minute that this flower is this protein.
It's called the amyloid precursor protein,
or APP.
APP is a useful protein, it helps neurons when they grow.
But it has one major problem:
it has a very dangerous part that has many thorns,
that goes, let's say, from here to there.
When everything's fine, like in the brain of a young and healthy person,
APP gets cut in the middle of its dangerous part,
releasing two harmless fragments.
But in the brain of a person who has Alzheimer's disease,
two other enzymes become more active,
and they cut APP at the top of the dangerous part,
and at the bottom, like this,
releasing, as you can see, intact
this dangerous part, which is called the Abeta fragment.
This wouldn't be a problem
if it happened to only one APP molecule.
But the problem is it happens to many APP molecules.
And the obsession of Abeta fragments is to aggregate,
which means that they group together, like this,
and form thorny bundles aggressing the neuron.
This is one example of a protein involved in Alzheimer's disease.
There are other proteins that are involved.
Some are even involved in several diseases,
such as, for example, the prion protein,
which is the primary player in prion diseases,
such as mad cow disease, or Creutzfeldt-Jakob disease,
or a protein named tau,
which is also involved in frontotemporal dementia.
The protein tau, for example, stabilizes tube-like structures
that are necessary for maintaining the neuron's shape
and transporting little vesicles containing useful molecules
to its extremities.
In Alzheimer's disease, the tau protein gets modified,
aggregates like Abeta did,
detaches from the tube-like structures which damage the neuron.
Of course, there are still many missing pieces in the puzzle,
gaps in knowledge that scientists continue to work on,
and it's extremely important to continue this basic research to advance knowledge.
But we already have a roadmap of what's happening.
And this roadmap indicates several critical steps in the disease process,
several proteins or pathways,
that will serve as targets for therapeutic agents.
In other words,
we have a handle on how to develop disease-modifying treatments.
So, now, what about the other diseases?
Parkinson's, Huntington's, prion diseases?
I don't have the time to specifically explain
what's going wrong in the brains of these patients.
But the bottom line is that these diseases are also caused by specific proteins
that misbehave and aggregate,
and that we have identified a number of critical steps in the disease processes
to allow for the development of disease-modifying therapies.
Now, this was all about the progress we've made
in understanding these diseases.
But, at the same time,
huge advances have been made in the field of drug discovery.
We know better how to block a specific protein
or even reduce its amount.
We can screen hundreds of thousands of molecules per day
in the search for those exhibiting the desired property.
And chemists are inventing continuously new methods to modify molecules
and make them better drugs.
Plus, we have made leaps in the field of regenerative medicine and stem cells.
Do you know, for example,
that it is possible to take a cell from the skin
and transform it into a neuron?
So here's an idea worth spreading:
it's no longer time to just hope for cures of neurodegenerative diseases;
it's time to hurry on the road
that has unfolded and continues to unfold in front of us.
Scientists know what to do to develop these cures,
but they need your support.
Anyone of us has the power
to influence where our society, where our world, is headed.
Take the time to think where you want us to go.
And you might already know what you can do to help.
Or you might discover it later.
But, in any case,
if all of us think that it is a worthwhile cause
preventing 100 million people from getting Alzheimer's disease by the year 2050,
then Zack will never have to worry about
not finding his way back home from a bicycle ride.
(Applause)