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[Music]
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scientists think they found the Fountain
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of Youth what I think will become the
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cover story on magazines that humans
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have discovered the Fountain of Youth
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and this will arise from yamanaka Factor
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based cell reprogramming methods it
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feels like a piece of technology that's
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fallen through a wormhole from the
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future it does sound a little bit like
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science fiction A3 billion investment
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that was just made in Altos Labs which
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is probably one of the biggest seed
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Investments ever he has made seminal
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contributions to understanding stem cell
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reprogramming so at this time it's my
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pleasure to introduce our uh recipient
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this year Juan Carlos espia
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[Music]
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[Applause]
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[Music]
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belante good afternoon my name is Juan
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Carlos
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Belmonte I'm going to start my
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participation with a rather provocative
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question which is
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can we rejuvenate an
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organism and if so what is the
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implication of that respon for human
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health for human
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disease so the the book of Our Lives is
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given to us when we are born our parent
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past has this set of instruction these
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millions and millions of letters that
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constitute our
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genome and by and large this is a very
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solid process but every now and then
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there is mistakes in these
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letters and they may have importance for
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our life or may be
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irrelevant let me give you an example
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for instance you change in this
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case a c to a
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t you're going to have a phenotype that
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is depe here the these kids they are in
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the picture between 6 and 10 years old
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but they look much older they're really
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all and they're not going to pass their
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teenage H age and just because of this
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small mutation a c into a
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t now fortunately in the last few years
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we scientists have developed method by
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which we can reverse that change we can
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fix that mistake and for instance we
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have models in the lab we have animal
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models in this case is a mouse where we
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have created the same
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mutation the C into a t and this mouse a
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lab mouse lives for about 2 years this
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mouse will live just for a couple of
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month three four months maximum and it
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will have the same accelerated aging
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process of the human but we can fix this
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we can change this T back into a c and
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we get this mouse which has nothing to
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do with the previous Mouse is healthier
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live longer and is able to regenerate
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some of their tissues that before it
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couldn't do
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it the problem as I was indicating
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before is that
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um this is a very small percentage of
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the mistakes that happen in our life by
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and large this is less than 1% there is
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mistakes that generate diseases like
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this by and large we have many other
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diseases that are not due to a mutation
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in our
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genome and if we look at this graphic
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that represent age and the possibility
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of
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death you can see that after certain
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number of years around 4
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45 the major risk factor for getting any
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disease is precisely that years
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age so the
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longer we live The increased risk to get
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diseased and around 40 45 we start to
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develop all these diseases that you see
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at the top of the
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screen and they are not related to
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changes into C or a t or a particular
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mutation so how this
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happen how these diseases appear and
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what can we do about reversing these
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diseases so let's go down to the cell
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level here you have two type of cells a
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very young cell healthy
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cell and an all an unhealthy
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cell the healthy cell is very res
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resilien in the presence of risk factors
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it has a very strong buffer capacity we
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call that that can deal with
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these these stresses however the all an
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unhealthy cell in addition to the fact
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that has been exposed because of time to
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more factors excuse me it has less
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buffer capacity it's less resilient to
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these factors that damage reach the
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cell and the question
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that I want to present today has to deal
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with this buffer capacity and what is
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buffer capacity let's see if I can
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explain this well so with time as time
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passes there is more risk factors during
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normal aging there is more stress and
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the buffering capacity the resilient of
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these cells goes go down and when these
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two arrows these two curve mix the Seas
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appear and the question is can we
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increase buffer capacity so that then
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the disease appears later or it never
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appear can we increase the cell
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resilience to deal with the disease that
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appearing with aging when we are
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young we really don't think about AG
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when we are all a big percentage of our
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days is just thinking how bad I feel and
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what can I do so can we increase this
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buffer capacity so that disease doesn't
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appear it takes longer to appear or we
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can even reverse it and how can this be
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done just pause for a moment what is
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aging what makes that cell fragile
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unhealthy many things our metab po
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change with
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ag our energy levels drop our
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mitochondria don't produce that ATP that
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is needed for the cell to work
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properly stem cells in our body die many
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things happen while we
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age but I'd like to Poe the idea that
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among all these things that happen
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during aging there is one very important
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thing that could help to increase this
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buffer capacity and this has to do with
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what we call the epig
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genome Epi comes from the Greek above
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above our genome above the instructions
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that we receive from our
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parents and if we look at the cell and
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the The genome the DNA of of any cell is
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is very big it will take approximately 6
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ft if we were to extend it
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here but we need to pack it inside a
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cell and it has a special
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conformation bounded by the specific
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proteins which in a very basic way we
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can divide it in in a confirmation that
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is open for business that we call open
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chromatin or close for business close
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chromatin and just this changing the
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conformation of the chromatine may have
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huge effect in the health
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of the cell and the
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organism in the time when the disease
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appears and the first and most important
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experiment to demonstrate this was done
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by Dr s
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yamanaka where what he did was a very
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simple experiment he took four
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genes added to an adult cell a cell that
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is fragile that is
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unhealthy and make that cell an
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embrionic like cell
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again and he did this by changing this
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confirmation of the
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chromatin now can this help us this
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experiment for which he was awarded the
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Noel price can this help us deal with
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the problem I am trying to convey today
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reverse disease bring back time and make
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the cell more resilient and healthy
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again so through a few years of studies
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the message is this that there is a
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correlation between the conformation of
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the chromatin aging and disease when the
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epigenome when the chromatine is closed
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we call this
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heterochromatin the cell is Young is
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healthy when the chromatin is open it
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leads
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to the increase the loss of buffer
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capacity and therefore disease and aging
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and the question is can we reverse that
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can we this correlation can we do
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something to alter the confirmation of
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this chromatin and demonstrate that just
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by bringing an open chromatine to a
00:10:11
closed chromatine we can rejuvenate a
00:10:14
cell and how do we do that we took
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advantage
00:10:20
of the initial ideas and studies of s
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yamanaka and using again this mouse
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model that I indicated before this
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animal that has a
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mutation that has a c into a te that
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leads to an accelerated aging you can
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see the animal here doesn't have hair
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it's small it's not going to leave for
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too long and what we did we took these
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four factors So-Cal yamanaka factors and
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put it inside this mouse this old mouse
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we're not fixing the mutation remember
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at the beginning there is Technologies
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by which we can fix the mutation what
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we're doing here is just altering the
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chromatin the mutation is still there in
00:11:08
this mouse the cause of the problem that
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letter is still there not fixed but
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we're altering the
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chromatin and we do this not
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continuously we just do short pulses of
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the yamanaka factors we put just during
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the weekend we put these factors not
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during the entire week to this mouse and
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what happen is that we get a very
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different Mouse healthy mouse that is
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able to live
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longer and remember we have not fixed
00:11:37
the mutation the te is still there so
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just by this small change in the
00:11:44
chromatin we can rejuvenate a
00:11:48
mouse and here is the just example of
00:11:52
what I'm telling you we can either with
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very precise tools that we have
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developed correct bre a specific
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mutation at the top the C to a t or
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without knowing the mutation just that
00:12:07
we know that this Mouse has a problem we
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just alter the status of the chromatine
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and we practically get the same
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phenotype we get Rejuvenation on this
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mouse either genome correction or
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epigenome buffering increasing the
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capacity the buffering capacity of this
00:12:27
mouse so we have gone through from the
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initial point to a later point where the
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mouse will live longer and will have a
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healthier
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life now anyone could tell me yes you
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are telling me just about one case this
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particular mouse that has this mutation
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does it work for something else for
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other
00:12:50
diseases and the answer is yes let me
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tell you just one more example and a few
00:12:56
others in a summary here we have another
00:12:59
mutation these mice have a mutation in a
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gene called
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leptine which make these mice eat all
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the time and as such they get fat they
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change their metabolism they get older
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faster Etc if we just give a short pulse
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of these yamanaka factors we get this
00:13:20
mouse the mouse still keeps eating
00:13:22
because it has the mutation we haven't
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corrected but the mouse now has less fat
00:13:28
in the the liver and can respond to
00:13:31
glucose like a
00:13:33
normal young and healthy
00:13:35
Mouse and if we extend now and I don't
00:13:38
have time to go through this to many
00:13:40
other diseases that we have test in the
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lab kidney disease skin disease liver
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disease muscle disease Etc the same
00:13:50
thing happen we can bring back this
00:13:53
buffer capacity and make the cell
00:13:55
younger and the mouse younger
00:14:00
there's a sentence there that says a
00:14:02
deceased agnot this approach when you
00:14:05
are you have a problem you have a
00:14:08
disease you go to the doctor and it give
00:14:11
you a medicine but if you have another
00:14:14
disease it give you another medicine if
00:14:16
we have a mouse with a mutation we try
00:14:19
to correct that mutation another mouse
00:14:22
with another disease we correct that
00:14:24
mutation but what I'm telling with this
00:14:26
slide is that independent of the disease
00:14:30
just by this small switch of changing
00:14:33
the chromatin we can
00:14:37
increase the capacity of resilience of
00:14:40
this mouse so that the disease takes
00:14:43
longer or is even
00:14:46
reverse I think this is a very profound
00:14:49
message that is not very precise we are
00:14:53
not touching the genome we're touching
00:14:55
the epigenome but without this Deion we
00:15:00
can revert
00:15:01
disease now the key question is this is
00:15:04
great I told you can we rejuvenate an
00:15:06
organism at the beginning it seems that
00:15:10
based on this and other
00:15:12
experiments in Rodin in the lab the
00:15:15
answer is yes we take mice with
00:15:17
different pathologies we pass them
00:15:20
through these short pulses of yamanaka
00:15:22
factors and they they're better the the
00:15:26
disease takes longer to appear they live
00:15:28
longer
00:15:30
but even though in science this this
00:15:33
animal is the one that we know more
00:15:34
about health and disease much more than
00:15:37
humans our interest is healthy people
00:15:42
would this work in humans and this is
00:15:46
our mission in Aldos try to by this
00:15:51
cellular Rejuvenation
00:15:54
programming increase the buffer capacity
00:15:56
of a human cell so that the Sease is
00:16:00
reversed or can take longer to
00:16:03
appear we have done this in isolated
00:16:07
human cells in the
00:16:09
petrides but the next step is to move to
00:16:12
a human being an entire organism like
00:16:15
the
00:16:16
mouse and this has to be done so that
00:16:19
there is with all the safety and all the
00:16:22
precautions so that we do not harm when
00:16:26
this experiment is done these mice are
00:16:28
healthy healthy they're fine there is
00:16:30
nothing wrong with them but we need to
00:16:32
really be very cautious when touching a
00:16:37
human
00:16:38
cell so rather than delivering these
00:16:42
factors inside inv Vivo of a human being
00:16:47
what if we do it ex Vio and here is an
00:16:51
example organ transplant we know that
00:16:55
organ donations save thousands and
00:16:57
thousands of lives every year in our
00:17:01
planet but nonetheless there are many
00:17:05
thousands of organs that are discarded
00:17:08
because their quality because they are
00:17:10
all the doctor when the organ
00:17:14
comes look at the organ and said this is
00:17:17
this organ is not good enough doesn't
00:17:19
have enough quality to be transplanted
00:17:22
and it just get
00:17:24
discarded what if instead of going
00:17:27
directly into a human being we try to
00:17:30
rejuvenate this organ that is
00:17:32
discarded and see if the doctor now will
00:17:35
say now this organ is ready to be
00:17:38
transplanted whatever conditions and
00:17:40
quality requir by this doctor and we are
00:17:43
making progress into this area you can
00:17:47
see here when we
00:17:50
transplant ER in this case is still in
00:17:53
Rodin an all
00:17:56
kidney into a young rat and we compare
00:18:00
this with the transplantation of a young
00:18:02
kidney the life of the horse is very
00:18:05
different you see these two the green
00:18:08
and the blue lines so the
00:18:12
blue line is with no treatment the green
00:18:16
line is after a short pulse of these
00:18:19
factors that is given X Vivo to this
00:18:23
organ before it's transplanted and that
00:18:25
lead to an increase in the survival of
00:18:28
the hor so that's one way to start
00:18:32
approaching of moving this technology
00:18:35
that we are developing in the lap in
00:18:36
mice into humans but at the same time
00:18:41
there's one thing that and I'm finishing
00:18:43
there is one thing that I would like to
00:18:46
stress it's not that all the cells of
00:18:50
our organism go bad with time otherwise
00:18:53
we'll be dead there just a few cells and
00:18:57
with time there is more and more of
00:18:59
these fragile unhealthy cells that don't
00:19:02
have enough buffer capacity and you can
00:19:05
see this in this diagram the blue dots
00:19:08
indicate that with time we have more and
00:19:11
more of these nonfunctional cells but
00:19:14
what we don't want to touch is what is
00:19:17
working we don't want to deliver these
00:19:20
factors to cells that are healthy and
00:19:23
that are
00:19:24
functional how do we deliver these
00:19:26
factors just to those cells that are not
00:19:28
work work into these blue cells so you
00:19:31
see here the two H situation in a y
00:19:35
tissue you almost don't have any of
00:19:37
these fragile and healthy cells and how
00:19:40
can we deliver the factors just in the
00:19:44
age situation to the unhealthy cells but
00:19:47
we don't touch we don't want to touch
00:19:49
the healthy cells and this is what we we
00:19:52
have been doing there is a specific
00:19:55
genes and markers that Target and
00:19:58
identify by the unhealthy cell and with
00:20:01
these markers we can guide our yamanaka
00:20:04
factors just to the unhealthy cell and
00:20:07
we obtain the same phenotype you can see
00:20:09
here an increase in life span just
00:20:12
targeting the unhealthy cell increasing
00:20:15
the buffering capacity of the unhealthy
00:20:17
cell and the last slide that I want to
00:20:20
show you is for instance an organ like
00:20:23
the skin if we bring these factors to
00:20:28
the non healthy cell of the skin you see
00:20:31
phenotypes like this for instance an old
00:20:33
mouse like us with time will get gray
00:20:37
hair it would just bring the factors to
00:20:41
the unhealthy cells of the of the skin
00:20:44
that
00:20:46
produce this deterioration of function
00:20:50
now you see that the gray hair doesn't
00:20:53
appear or if we do a wound in the skin
00:20:56
of an animal of an animal and this in us
00:21:02
after a certain age the wound takes a
00:21:05
long time to close or even it doesn't
00:21:08
close you can see at the top the
00:21:09
nontreated in red there is there is a
00:21:12
wound there that has doesn't heal while
00:21:16
the treated one even in a very very old
00:21:19
mouth it just make a perfect Skin So
00:21:23
summary of what I have told you today is
00:21:26
this that
00:21:28
there is what we call Precision Medicine
00:21:31
by which we
00:21:33
can fix some of these mutations errors
00:21:37
that our parent transmit into the book
00:21:40
of our life but that's less than 1% of
00:21:43
the diseases the majority of diseases
00:21:46
correlate with
00:21:48
age passing of the time and they don't
00:21:51
have anything to do with particular
00:21:55
mutations and without touching the
00:21:57
genome with this Precision medicine just
00:22:01
just modifying the conformational
00:22:04
structure of the chromatin we can bring
00:22:08
a disease and aged cell into a cell that
00:22:12
is more resilient and more functional
00:22:15
and certainly this type of experiment
00:22:18
and the messages that it open up the
00:22:21
question of can we rejuvenate a human
00:22:24
being and can we reverse diseas in human
00:22:27
thank you for your
00:22:28
[Applause]
00:22:39
right ju caros thank you for the
00:22:42
presentation I want to I I don't I don't
00:22:44
know if you can
00:22:45
overstate the significance of the
00:22:48
discovery you have made and it's funny
00:22:51
to me how it's not popular uh knowledge
00:22:55
at this point because of the results
00:22:58
that you and other
00:23:00
scientists have collected and the impact
00:23:02
it will have to literally restore uh
00:23:06
cellular health and and deage an
00:23:09
organism and um the yamanaka factors or
00:23:13
four proteins just just for Layman's
00:23:15
conversation there are four proteins
00:23:17
that's what a factor is it's a A protein
00:23:21
that causes a change in the epigenome
00:23:23
and unwinds parts of the DNA and as a
00:23:25
result new genes get turned on other
00:23:27
genes get turned off and the cell kind
00:23:29
of revitalizes it becomes young
00:23:32
again um you discovered that you can
00:23:37
actually and and they did this all the
00:23:38
and made the cells go back all the way
00:23:39
to being stem cells but what you
00:23:41
discovered was the ability to partially
00:23:43
ReStore youthfulness in the cells
00:23:45
through partial reprogramming and that's
00:23:47
a dose Factor you put a smaller amount
00:23:50
of the yanaka factors on the cells what
00:23:52
how do you control it and then I want to
00:23:53
ask a question um about if you put too
00:23:57
much does it then because I know there's
00:23:58
been tests in mice where you end up with
00:24:00
cancer because then the cells start
00:24:01
multiplying too quickly so maybe you can
00:24:02
tell us a little bit about what it means
00:24:03
to do partial reprogramming with the
00:24:06
amak what does partial mean very
00:24:09
important question thank you for let's
00:24:12
see if I can clarify this what Dr s
00:24:15
yamanaka did is something that we no one
00:24:18
in in science in general could believe
00:24:21
that you can bring an adult
00:24:24
cell to a start life again become an
00:24:30
embryo cell embryol likee cell an
00:24:33
embryonic stem cell can be whatever we
00:24:36
have more than 250 cell types in our
00:24:40
body our skin cell is different than our
00:24:43
eye cell is different than our brain
00:24:44
cell because different genes are turned
00:24:46
on and off in each of those cells they
00:24:49
have the same DNA but they have a
00:24:50
different epigenome different genes are
00:24:52
turned on perfectly explained thank you
00:24:54
so and
00:24:56
what I think it's so for people to get
00:24:59
that yeah what SAA did was just to
00:25:02
delete delete all that information the
00:25:04
identity of a skin cell of a heart cell
00:25:08
and bring it back to the very beginning
00:25:10
to the to the very first time when we
00:25:13
are born to this type of cells
00:25:16
now is when he was putting these factors
00:25:20
it's his factors the yamanaka factor for
00:25:22
a long time four proteins for four prot
00:25:25
four proteins put them on the cell this
00:25:26
happens now we don't want this imagine
00:25:30
if we were to put this in the
00:25:32
heart the key cell in the heart is
00:25:34
called cardom myosite and what it does
00:25:37
is beat so if we remove the identity
00:25:41
can't of that cell is not anymore a
00:25:44
cardom myosite and go back to an
00:25:46
embryonic cell the heart is not going to
00:25:50
beat if we do that in the liver theoy is
00:25:54
not going to do its function so doing
00:25:58
this going back in in time to really the
00:26:01
earli
00:26:03
stages it will not do good to our bodies
00:26:08
and then and cancer arises and then if
00:26:10
you bring and lose the identity of a
00:26:12
particular cell then you are open for
00:26:15
that cell to become something else right
00:26:18
like a cancer cell or a skin cell is
00:26:21
transformed into aite many wrong things
00:26:24
could happen we want to maintain the
00:26:27
identity of this cell
00:26:29
and the small switch here that we did as
00:26:32
you are asking me is rather than having
00:26:35
the factors for a long time we just gave
00:26:37
a short
00:26:39
pulse what that is doing is altering the
00:26:44
chromatin but for a very short time it's
00:26:47
a small shock and then the chromatin get
00:26:49
close and maintain its
00:26:53
identity the cardiomyocyte is a cardom
00:26:56
myosite has not gone back
00:26:59
to a different cell typee but its
00:27:01
function is much better this is so the
00:27:04
idea is just a short P of these proteins
00:27:07
which by the way these are the proteins
00:27:10
that s yamanaka discovered but I'm
00:27:12
convinced that there will be many other
00:27:15
proteins so that's organism that's the
00:27:17
next thing I wanted to ask you so it
00:27:19
sounds like the search is on in various
00:27:21
startups at Alto slabs for other
00:27:24
proteins that can do this but perhaps
00:27:27
not protein but smaller molecules
00:27:30
peptides or small molecules where
00:27:33
theoretically you could take a
00:27:35
pill and it would do the same thing is
00:27:40
that a
00:27:42
reality so I think that one of the
00:27:46
biggest inventions that we humans have
00:27:48
made is the place we're here today the
00:27:52
university the Curiosity the knowledge
00:27:55
to advance in things that we don't
00:28:00
understand um
00:28:02
and discovering what other proteins what
00:28:05
other factors could do the same thing
00:28:08
belongs to that domain of the Curiosity
00:28:11
and trying to increase our knowledge but
00:28:14
many times we need to try to apply this
00:28:16
knowledge and you're asking me how are
00:28:19
you going to deliver whatever factors
00:28:22
you discover into a human
00:28:24
being you can do this in the lab with
00:28:27
many other ways but ideally you would
00:28:29
like to just put that into
00:28:32
appeal and so here is where the other
00:28:35
important thing come and that's
00:28:39
industry by mixing the Bas
00:28:43
of
00:28:45
Academia this curiosity this trying to
00:28:48
understand how we can close and open the
00:28:49
chromatin with many other
00:28:52
factors with the experience the drive
00:28:55
and the focus of
00:28:57
Industry can we answer the question that
00:28:59
you are asking can we put these factors
00:29:02
or any other factors that alter the
00:29:05
chromatine into appeal this is precisely
00:29:09
our Endeavor try to make this safe and
00:29:12
available to can I ask you a more maybe
00:29:16
a more basic
00:29:17
question um if this buffer
00:29:22
capacity is essentially the insulation
00:29:25
that we are born with that then decays
00:29:27
so
00:29:28
young cell good buffer capacity old cell
00:29:31
no buffer capacity in very simple terms
00:29:33
based on your side what is the
00:29:37
scientific community's understanding
00:29:40
about how to minimize the rate of change
00:29:44
and the Decay by things that people in
00:29:47
this room can control where we live the
00:29:49
things that we're exposed to our food
00:29:51
supply do any of those things to your
00:29:55
understanding have an impact that's
00:29:57
measurable
00:29:59
and achievable by us today while we wait
00:30:01
for altos and others to deliver more
00:30:03
chemical manipulation of this huge
00:30:05
impact incredible question and really
00:30:08
huge impact just think of exercise we
00:30:11
have compare what are the changes in the
00:30:14
Cell between
00:30:17
exercise and the short pulses of Y Mana
00:30:20
factors and you couldn't believe the
00:30:23
similarities in the changes in gene
00:30:25
expression that exercise
00:30:28
th and how overlap these changes happen
00:30:33
when we do the yamanaka the sh PES of
00:30:36
yamanaka factors so things like exercise
00:30:40
but exercising what kind of exercise how
00:30:42
much how
00:30:43
often why you want to know the answer
00:30:45
too what don't laugh actually you know
00:30:47
what don't answer the question you can
00:30:49
tell us afterwards because they don't
00:30:50
care don't it's
00:30:51
[Applause]
00:30:53
fine and exercise things that your
00:30:56
mother will tell you eat less
00:31:00
exercise H when I say stress I mean it
00:31:03
stress to the cell that is going to
00:31:05
alter the epigenome so until we really
00:31:10
understand how these changes in
00:31:12
chromatine happen all these things that
00:31:15
we do sometime with our life really
00:31:18
improve the buffer capacity and has that
00:31:20
been published or studied in a way
00:31:22
that's digestible for Layman meaning
00:31:25
like whether it's intermittent fasting
00:31:27
or whether it's the the quantity of food
00:31:29
or whether it's you know specific forms
00:31:31
of exercise over another has that been
00:31:33
well studied enough that we can at a
00:31:36
minimum we can even just link to all of
00:31:37
this so that you guys can get this
00:31:39
information but is it out there this is
00:31:41
I would say the last 10 years have been
00:31:44
an
00:31:46
incredible jump into into these studies
00:31:50
so far most of them have been done in
00:31:53
animal models in the lab and we are
00:31:57
starting to translate this to humans um
00:32:01
for instance I just finish it's not I
00:32:06
think I can say that tomorrow it will be
00:32:08
just one of these molecules that
00:32:12
diabetic people take metformine to lower
00:32:15
down their glucose they can reprogram
00:32:18
the cells so that all the cognitive
00:32:21
function or not just rodents and this is
00:32:23
the key thing but of monkeys which are
00:32:27
99% % their book of life is very 99 9%
00:32:32
similar to us right it can reprogram
00:32:34
these cells and the cognitive abilities
00:32:37
of monkeys and their lifespan is
00:32:40
increased so this is coming this is not
00:32:44
something that is just this small Mouse
00:32:48
in the lab where we know a lot about
00:32:50
their health and disease but I feel the
00:32:53
next decade probably many of these
00:32:56
discoveries with the caveat that it's a
00:32:59
mouse and a mouse is not a human might
00:33:01
be translated to human you put a slide
00:33:03
up there where you had a obviously a
00:33:05
whole bunch of Target markets some were
00:33:08
autoimmune diseases some were cancers
00:33:11
some were more just general aging
00:33:15
um how do you decide or how do you
00:33:18
figure
00:33:19
out where there is the uh most real
00:33:24
application today because I part of it
00:33:26
is there's a obviously
00:33:28
Market issue of making sure you continue
00:33:30
to have capital and prove scientific
00:33:32
value but part of it is there may be
00:33:34
some small winds today in rare diseases
00:33:37
or something that could allow you to
00:33:39
commercialize this faster so how do you
00:33:41
think about which problems should come
00:33:47
first good question I put up there the
00:33:51
ex Vio example with the organ
00:33:56
transplant this is probably one of the
00:33:58
most cautious and safest safest approach
00:34:02
where say uh acute liver disease there's
00:34:07
nothing about this you're are going to
00:34:08
die in 3 days right and if an organ is
00:34:11
not there you can do nothing so acute
00:34:15
and and deadly diseases that could
00:34:18
happen could be an
00:34:20
initial um target for these type of
00:34:24
approaches um but again I I want to say
00:34:29
that even though we are trying to move
00:34:34
as fast as we can into humans and we are
00:34:36
doing this experimen in human cells in
00:34:39
the Petri a mouse is not a human and
00:34:42
this will need time to be replicated in
00:34:45
a human being before we wrap can we just
00:34:47
talk about how altto Labs is set up it's
00:34:51
probably got more funding than any other
00:34:53
private company in recent history it's
00:34:57
really incredible how the the maybe you
00:34:58
can tell us how how you've organized
00:35:00
this this work this Mission um and again
00:35:04
is reflecting on the importance that we
00:35:07
know so little and about the fundamental
00:35:11
science of what is behind this big
00:35:15
question is a question that we human
00:35:17
beings have have tried to approach since
00:35:20
ever how can we deal with disease with
00:35:24
aging so there is so many things we
00:35:27
don't no basic sign is needed so as a
00:35:30
startup you raised billions of dollars
00:35:32
to do a lot of core research as well as
00:35:35
product development and at the same time
00:35:37
in parallel yeah with all the safety
00:35:40
approaches that we can think of and we
00:35:43
were talking about one possible
00:35:45
example perhaps without knowing every
00:35:49
detail of how it works provided is safe
00:35:53
and could have a positive effect trying
00:35:55
to move this forward so it's a
00:35:57
combination of what we like to call the
00:36:01
base of basic science and the base of
00:36:04
Industry yeah well look I mean I don't
00:36:06
think there's a human on earth that will
00:36:08
uh not benefit and does not appreciate
00:36:11
the the effort and and obviously
00:36:12
everyone hopes that you guys are
00:36:15
extremely successful in both the
00:36:17
scientific and Commercial uh Pursuits I
00:36:20
it seems to me like as you guys have
00:36:22
your breakthroughs which I think you're
00:36:25
uh you're going to have given the
00:36:27
backing and people that are involved
00:36:29
over time uh partial cell reprogramming
00:36:33
could be one of the most profoundly
00:36:34
impactful technologies that humans have
00:36:38
ever discovered or invented so we
00:36:39
appreciate the work that you do and and
00:36:41
thank you for being here with us thank
00:36:43
you for thank you
00:36:46
[Applause]
