I'm very pleased to be here today to talk to you all about how we might repair the damaged brain, and I'm particularly excited by this field, because as a neurologist myself, I believe that this offers one of the great ways that we might be able to offer hope for patients who today live with devastating and yet untreatable diseases of the brain.
Veoma mi je drago što sam danas ovde da bih govorio kako bismo mogli popraviti oštećen mozak. Tim područjem sam izuzetno oduševljen jer kao neurolog, verujem da nudi sjajan način kojim bismo mogli ponuditi nadu pacijentima koji danas žive sa razornim i neizlečivim bolestima mozga.
So here's the problem. You can see here the picture of somebody's brain with Alzheimer's disease next to a healthy brain, and what's obvious is, in the Alzheimer's brain, ringed red, there's obvious damage -- atrophy, scarring. And I could show you equivalent pictures from other disease: multiple sclerosis, motor neuron disease, Parkinson's disease, even Huntington's disease, and they would all tell a similar story. And collectively these brain disorders represent one of the major public health threats of our time. And the numbers here are really rather staggering. At any one time, there are 35 million people today living with one of these brain diseases, and the annual cost globally is 700 billion dollars. I mean, just think about that. That's greater than one percent of the global GDP. And it gets worse, because all these numbers are rising because these are by and large age-related diseases, and we're living longer. So the question we really need to ask ourselves is, why, given the devastating impact of these diseases to the individual, never mind the scale of the societal problem, why are there no effective treatments?
Evo ovde je problem. Tu možete da vidite sliku nečijeg mozga s Alchajmerovom bolešću pored zdravog mozga. Kod Alchajmerove bolesti, okruženo crvenim, postoji vidljivo oštećenje - atrofija, stvaranje ožiljaka. Mogao bih vam pokazati jednake slike drugih bolesti: multiple skleroze (MS), bolesti motoričkih nerava, Parkinsonove bolesti, čak i Hantingtonove bolesti i sve one bi vam ispričale sličnu priču. Svim ovim poremećajima mozga je zajedničko da su jedna od najvećih pretnji javnom zdravstvu našeg doba. Ovde su brojevi zaista prilično poražavajući. U svakom momentu danas živi 35 miliona ljudi s jednom od tih bolesti mozga, a godišnji trošak na globalnoj ravni je 700 milijardi dolara. Razmislite o tome. To je više od jednog procenta globalnog BDP-a. I još se pogoršava, ti brojevi su u porastu, jer su to većinom bolesti starosti, a živimo duže. Tako moramo da se zapitamo, zašto, s obzirom na razorni uticaj tih bolesti na pojedinca, bez obzira na obim društvenog problema, zašto nema efikasnih terapija?
Now in order to consider this, I first need to give you a crash course in how the brain works. So in other words, I need to tell you everything I learned at medical school. (Laughter) But believe me, this isn't going to take very long. Okay? (Laughter) So the brain is terribly simple: it's made up of four cells, and two of them are shown here. There's the nerve cell, and then there's the myelinating cell, or the insulating cell. It's called oligodendrocyte. And when these four cells work together in health and harmony, they create an extraordinary symphony of electrical activity, and it is this electrical activity that underpins our ability to think, to emote, to remember, to learn, move, feel and so on. But equally, each of these individual four cells alone or together, can go rogue or die, and when that happens, you get damage. You get damaged wiring. You get disrupted connections. And that's evident here with the slower conduction. But ultimately, this damage will manifest as disease, clearly. And if the starting dying nerve cell is a motor nerve, for example, you'll get motor neuron disease.
Da biste to shvatili moraću vam dati ubrzani kurs o funkcionisanju mozga. Drugim rečima, moram vam ispričati sve što sam naučio na medicinskom fakultetu. (Smeh) Verujte mi, neće trajati dugo. U redu? (Smeh) Mozak je užasno jednostavan: sastoji se iz četiri ćelije, dve su ovde prikazane. Tu je nervna ćelija, a zatim mijelinski omotač, ili izolaciona ćelija. Zove se oligodendrocit. Kada te četiri ćelije rade zajedno u zdravoj harmoniji, stvaraju izvanrednu električnu simfoniju, i ta električna aktivnost podupire našu sposobnost razmišljanja, ispoljavanja emocija pamćenja, učenja, kretnji, osećaja itd. No, isto tako, svaka od te četiri ćelije sama ili zajedno, može da zastrani ili da odumre i kad se to dogodi, dobijete oštećenje. Imate oštećeno ožičenje. Imate poremećene veze. To se ogleda u sporijoj provodljivosti. Na kraju će se to oštećenje jasno manifestovati, kao bolest. Ako je nervna ćelija koja počinje da odumire motorički nerv, na primer, dobićete bolest motoričkih nerava.
So I'd like to give you a real-life illustration of what happens with motor neuron disease. So this is a patient of mine called John. John I saw just last week in the clinic. And I've asked John to tell us something about what were his problems that led to the initial diagnosis of motor neuron disease.
Želeo bih da vam dam realnu ilustraciju toga šta se događa kod bolesti motoričkih nerava. Ovo je moj pacijent po imenu Džon. Džona sam video prošle nedelje na klinici. Zamolio sam ga da nam kaže nešto o svojim problemima koji su doveli do početne dijagnoze bolesti motoričkih nerava.
John: I was diagnosed in October in 2011, and the main problem was a breathing problem, difficulty breathing.
Džon: Dobio sam dijagnozu u oktobru 2011. i glavni problem je bio u disanju, otežano disanje.
Siddharthan Chandran: I don't know if you caught all of that, but what John was telling us was that difficulty with breathing led eventually to the diagnosis of motor neuron disease.
SČ: Ne znam da li ste sve shvatili, Džon nam je rekao da je poteškoća s disanjem na kraju dovela do dijagnoze bolesti motoričkih nerava.
So John's now 18 months further down in that journey, and I've now asked him to tell us something about his current predicament.
Dakle Džon je sada 18 meseci dalje na tom putu i zamolio sam ga da nam kaže nešto o svojoj trenutnoj situaciji.
John: What I've got now is the breathing's gotten worse. I've got weakness in my hands, my arms and my legs. So basically I'm in a wheelchair most of the time.
Džon: Sada se disanje pogoršalo. Osećam slabost u šakama, rukama i nogama. Tako sam većinom u invalidskim kolicima.
SC: John's just told us he's in a wheelchair most of the time.
SČ: Džon nam je upravo rekao da je u invalidskim kolicima najvećim delom vremena.
So what these two clips show is not just the devastating consequence of the disease, but they also tell us something about the shocking pace of the disease, because in just 18 months, a fit adult man has been rendered wheelchair- and respirator-dependent. And let's face it, John could be anybody's father, brother or friend.
Ova dva snimka nam pokazuju ne samo poražavajuće posledice bolesti, već takođe šokantan tempo bolesti, jer je za samo 18 meseci, odrasla osoba u dobroj kondiciji postala zavisna od invalidskih kolica i respiratora. Realno gledano, Džon bi mogao biti bilo čiji otac, brat ili prijatelj.
So that's what happens when the motor nerve dies. But what happens when that myelin cell dies? You get multiple sclerosis. So the scan on your left is an illustration of the brain, and it's a map of the connections of the brain, and superimposed upon which are areas of damage. We call them lesions of demyelination. But they're damage, and they're white.
Eto to se desi kada motorički nerv odumre. No, šta se desi kada odumre mijelinski omotač? Dobijete multiplu sklerozu. Snimak na vašoj levoj strani je ilustracija mozga, to je mapa veza u mozgu, preko kojih su data područja oštećenja. Nazivamo ih lezije demijelinizacije, ali to su oštećenja i bela su.
So I know what you're thinking here. You're thinking, "My God, this bloke came up and said he's going to talk about hope, and all he's done is give a really rather bleak and depressing tale." I've told you these diseases are terrible. They're devastating, numbers are rising, the costs are ridiculous, and worst of all, we have no treatment. Where's the hope?
Znam o čemu sada razmišljate. Razmišljate: "O bože, ovaj je rekao da će govoriti o nadi, a sve što nam je do sada ispričao je prilično turobna i depresivna priča." Rekao sam vam da su ove bolesti užasne. One razaraju, brojevi rastu, troškovi su apsurdni, a najgore je od svega, što su neizlečive. Gde je tu nada?
Well, you know what? I think there is hope. And there's hope in this next section, of this brain section of somebody else with M.S., because what it illustrates is, amazingly, the brain can repair itself. It just doesn't do it well enough. And so again, there are two things I want to show you. First of all is the damage of this patient with M.S. And again, it's another one of these white masses. But crucially, the area that's ringed red highlights an area that is pale blue. But that area that is pale blue was once white. So it was damaged. It's now repaired. Just to be clear: It's not because of doctors. It's in spite of doctors, not because of doctors. This is spontaneous repair. It's amazing and it's occurred because there are stem cells in the brain, even, which can enable new myelin, new insulation, to be laid down over the damaged nerves. And this observation is important for two reasons. The first is it challenges one of the orthodoxies that we learnt at medical school, or at least I did, admittedly last century, which is that the brain doesn't repair itself, unlike, say, the bone or the liver. But actually it does, but it just doesn't do it well enough. And the second thing it does, and it gives us a very clear direction of travel for new therapies -- I mean, you don't need to be a rocket scientist to know what to do here. You simply need to find ways of promoting the endogenous, spontaneous repair that occurs anyway.
No, znate šta? Mislim da nade ima. Nade ima u ovom sledećem delu, ovog dela mozga kod drugog primera sa MS, jer to ilustruje da mozak može sam da se popravi. Jedino što to radi dovoljno dobro. Tu postoje dve stvari koje želim da vam pokažem. Pre svega radi se o oštećenju kod ovog pacijenta sa MS. Opet, to je još jedna od tih belih masa. Najbitnije je svetlo plavo područje okruženo crvenim. To svetlo plavo područje je nekad bilo belo. Bilo je oštećeno. Sada je sanirano. Da budem jasan: to nije zbog lekara. To je uprkos lekarima, a ne zbog njih. To je spontani popravak. Neverovatno je i desilo se zato što postoje matične ćelije u mozgu koje mogu da stvore novi mijelin, novu izolaciju, preko oštećenih nerava. Ovo je važno iz dva razloga. Prvo zato što je suprotno dogmi, kojoj smo se učili na medicini, bar ja, doduše u prošlom veku, koja glasi da se mozak ne regeneriše, za razliku od, recimo, kosti ili jetre. U stvari se regeneriše, jedino što to ne radi dovoljno dobro. A drugo je zato što nam to daje vrlo jasan pravac u potrazi za novim terapijama - hoću reći, ne morate biti genije da biste znali šta ovde da uradite. Jednostavno morate pronaći načine da podstaknete endogenu, spontanu sanaciju koja se i tako odvija.
So the question is, why, if we've known that for some time, as we have, why do we not have those treatments? And that in part reflects the complexity of drug development. Now, drug development you might think of as a rather expensive but risky bet, and the odds of this bet are roughly this: they're 10,000 to one against, because you need to screen about 10,000 compounds to find that one potential winner. And then you need to spend 15 years and spend over a billion dollars, and even then, you may not have a winner.
Ako to već izvesno vreme znamo, što je tačno, pitanje je zašto nemamo tih terapija? I to delimično odražava složenost u razvoju lekova. Razvoj lekova možete zamisliti kao prilično skup i riskantan ulog, a izgledi za taj ulog su u grubom ovakvi: 10.000 : 1, jer je potrebno proveriti oko 10.000 jedinjenja da bi se pronašao potencijalni pobednik. Zatim morate da potrošite 15 godina i više od milijardu dolara, pa čak i tada, možda nećete imati pobednika.
So the question for us is, can you change the rules of the game and can you shorten the odds? And in order to do that, you have to think, where is the bottleneck in this drug discovery? And one of the bottlenecks is early in drug discovery. All that screening occurs in animal models. But we know that the proper study of mankind is man, to borrow from Alexander Pope. So the question is, can we study these diseases using human material? And of course, absolutely we can. We can use stem cells, and specifically we can use human stem cells. And human stem cells are these extraordinary but simple cells that can do two things: they can self-renew or make more of themselves, but they can also become specialized to make bone, liver or, crucially, nerve cells, maybe even the motor nerve cell or the myelin cell. And the challenge has long been, can we harness the power, the undoubted power of these stem cells in order to realize their promise for regenerative neurology?
Dakle, pitamo se, možete li promeniti pravila igre i skratiti izglede? Da biste to učinili, morate promisliti gde je usko grlo u ovom otkrivanju leka? Jedno od uskih grla je u početku otkrivanja leka. Sva ta provera se odvija na životinjskim modelima. Znamo da je za pravo proučavanje čovečanstva potreban čovek, prema rečima Aleksandra Poupa. Dakle pitanje je, možemo li proučavati ove bolesti koristeći ljudski materijal? Naravno da to apsolutno možemo. Možemo da koristimo matične ćelije i posebno ljudske matične ćelije. Ljudske matične ćelije su te izvanredne i jednostavne ćelije koje mogu da urade dve stvari: mogu da se same obnavljaju ili da se nadgrađuju, ali mogu takođe da se specijalizuju da stvaraju kost, jetru ili, što je najvažnije, nervne ćelije, možda čak i motoričke nervne ćelije ili mijelinski omotač. Izazov postoji već dugo - da li možemo zauzdati moć, nespornu moć tih matičnih ćelija da bismo ostvarili to što one obećavaju u regenerativnoj neurologiji?
And I think we can now, and the reason we can is because there have been several major discoveries in the last 10, 20 years. One of them was here in Edinburgh, and it must be the only celebrity sheep, Dolly. So Dolly was made in Edinburgh, and Dolly was an example of the first cloning of a mammal from an adult cell. But I think the even more significant breakthrough for the purposes of our discussion today was made in 2006 by a Japanese scientist called Yamanaka. And what Yamaka did, in a fantastic form of scientific cookery, was he showed that four ingredients, just four ingredients, could effectively convert any cell, adult cell, into a master stem cell. And the significance of this is difficult to exaggerate, because what it means that from anybody in this room, but particularly patients, you could now generate a bespoke, personalized tissue repair kit. Take a skin cell, make it a master pluripotent cell, so you could then make those cells that are relevant to their disease, both to study but potentially to treat. Now, the idea of that at medical school -- this is a recurring theme, isn't it, me and medical school? — would have been ridiculous, but it's an absolute reality today. And I see this as the cornerstone of regeneration, repair and hope.
Mislim da to sada možemo, zbog nekoliko velikih otkrića u poslednjih 10, 20 godina. Jedno od njih je bilo ovde u Edinburgu i to je verovatno jedina slavna ovca, Doli. Dakle, Doli je stvorena u Edinburgu, i bila je primer prvog kloniranja sisara iz ćelije odrasle jedinke. Mislim da je još važnije otkriće za našu današnju raspravu napravio 2006. japanski naučnik po imenu Jamanaka. Jamanaka je, u fantastičnoj naučnoj kuhinji, pokazao da četiri sastojka, samo četiri sastojka, mogu efikasno da pretvore bilo koju adultnu ćeliju u pluripotentnu matičnu ćeliju. Značaj toga je teško preuveličati, jer to znači da je sada od bilo koga u ovoj sobi, a posebno od pacijenata, moguće stvoriti po meri personalizovan komplet tkiva za popravku. Uzmete ćeliju kože, pretvorite je u pluripotentnu ćeliju da biste mogli da napravite one ćelije koje su relevantne za bolest, za proučavanje i za potencijalno lečenje. Ta bi ideja na medicinskom fakultetu - ova se tema ponavlja, zar ne, ja i medicinsko školovanje? - bila smešna, iako je to apsolutna stvarnost danas. To vidim kao temelj regeneracije, popravke i nade.
And whilst we're on the theme of hope, for those of you who might have failed at school, there's hope for you as well, because this is the school report of John Gerdon. ["I believe he has ideas about becoming a scientist; on his present showing this is quite ridiculous."] So they didn't think much of him then. But what you may not know is that he got the Nobel Prize for medicine just three months ago.
I dok smo kod nade, za vas koji možda niste uspeli u školi ima nade i za vas, jer je ovo školski izveštaj Džona Gurdona. Nisu ga baš previše cenili tada. Možda ne znate da je dobio Nobelovu nagradu za medicinu pre samo tri meseca. I da se vratimo na prvobitni problem,
So to return to the original problem, what is the opportunity of these stem cells, or this disruptive technology, for repairing the damaged brain, which we call regenerative neurology? I think there are two ways you can think about this: as a fantastic 21st-century drug discovery tool, and/or as a form of therapy. So I want to tell you a little bit about both of those in the next few moments.
kakva je mogućnost tih matičnih ćelija ili te disruptivne tehnologije, za popravljanje oštećenog mozga, koju nazivamo regenerativnom neurologijom? Mislim da postoje dva načina razmišljanja o tome: kao o fantastičnom sredstvu 21. veka za otkrivanje lekova, i / ili kao o obliku lečenja. U nastavku ću vam govoriti nešto malo o obe stvari. Otkrivanje lekova u posudi - tako često
Drug discovery in a dish is how people often talk about this. It's very simple: You take a patient with a disease, let's say motor neuron disease, you take a skin sample, you do the pluripotent reprogramming, as I've already told you, and you generate live motor nerve cells. That's straightforward, because that's what pluripotent cells can do. But crucially, you can then compare their behavior to their equivalent but healthy counterparts, ideally from an unaffected relative. That way, you're matching for genetic variation.
o tome ljudi govore. Vrlo je jednostavno: recimo od pacijenta koji ima bolest motoričkih nerava uzmete uzorak kože, uradite pluripotentno reprogramiranje, kao što sam već rekao i stvorite žive ćelije motoričkih nerava. To je jasno, jer to pluripotentne ćelije mogu da urade. Presudno je da onda možete uporediti njihovo ponašanje u odnosu na njihov ekvivalent, zdravi pandan, idealno bi bilo od zdravih rođaka. Na taj način upoređujete genetske varijacije. Upravo to smo napravili ovde
And that's exactly what we did here. This was a collaboration with colleagues: in London, Chris Shaw; in the U.S., Steve Finkbeiner and Tom Maniatis. And what you're looking at, and this is amazing, these are living, growing, motor nerve cells from a patient with motor neuron disease. It happens to be an inherited form. I mean, just imagine that. This would have been unimaginable 10 years ago. So apart from seeing them grow and put out processes, we can also engineer them so that they fluoresce, but crucially, we can then track their individual health and compare the diseased motor nerve cells to the healthy ones. And when you do all that and put it together, you realize that the diseased ones, which is represented in the red line, are two and a half times more likely to die than the healthy counterpart. And the crucial point about this is that you then have a fantastic assay to discover drugs, because what would you ask of the drugs, and you could do this through a high-throughput automated screening system, you'd ask the drugs, give me one thing: find me a drug that will bring the red line closer to the blue line, because that drug will be a high-value candidate that you could probably take direct to human trial and almost bypass that bottleneck that I've told you about in drug discovery with the animal models, if that makes sense. It's fantastic.
u saradnji sa kolegama: u Londonu, Kris Šou, u SAD-u, Stiv Finkbejner i Tom Maniatis. Zanimljivo je da gledate žive, rastuće, motoričke nervne ćelije kod pacijenta s bolešću motoričkog neurona. Ovo je nasleđen oblik. Zamislite samo. Pre 10 godina bi to bilo nezamislivo. Pored toga što ih vidimo kako rastu izvan procesa, možemo ih napraviti fluorescentnim, no najvažnije je što onda možemo da pratimo njihovo pojedinačno zdravlje i upoređujemo bolesne ćelije motoričkog nerva sa zdravim. A kada sve to uradite i sastavite, shvatite da bolesne ćelije, pokazane u crvenoj liniji, imaju dva i po puta veću verovatnoću smrtnosti od zdravih. Pri tom je ključno da tada imate fantastičan rezultat analize za otkrivanje lekova, jer to što biste tražili od leka možete putem visoke propusne moći automatizovanog sistema proveravanja da tražite - daj mi jednu stvar: pronađi mi lek koji će crvenu liniju približiti plavoj, jer će taj lek biti kandidat visoke vrednosti koji biste verovatno mogli dati direktno na ispitivanje na ljudima i skoro zaobići usko grlo o kom sam vam govorio u otkrivanju lekova sa životinjskim modelima, ako bi to bilo smisleno. To je fantastično.
But I want to come back to how you might use stem cells directly to repair damage. And again there are two ways to think about this, and they're not mutually exclusive. The first, and I think in the long run the one that will give us the biggest dividend, but it's not thought of that way just yet, is to think about those stem cells that are already in your brain, and I've told you that. All of us have stem cells in the brain, even the diseased brain, and surely the smart way forward is to find ways that you can promote and activate those stem cells in your brain already to react and respond appropriately to damage to repair it. That will be the future. There will be drugs that will do that.
Ali vratiću se na temu kako biste mogli koristiti matične ćelije direktno za popravljanje oštećenja. I tu postoje dva načina za razmišljanje, koji se međusobno ne isključuju. Prvi, koji mislim da će nam na duge staze dati najveću korist, iako se na taj način još ne razmišlja, je razmisliti o onim matičnim ćelijama koje su već u mozgu, što sam vam već rekao. Svi mi imamo matične ćelije u mozgu, čak i oboleli mozak, i sigurno je pametan put napred pronalaženje načina da se podstaknu i aktiviraju te ćelije u vašem mozgu da bi reagovale i odazvale se adekvatno na oštećenja u cilju popravljanja. To će biti u budućnosti. Postojaće lekovi koji će to učiniti.
But the other way is to effectively parachute in cells, transplant them in, to replace dying or lost cells, even in the brain. And I want to tell you now an experiment, it's a clinical trial that we did, which recently completed, which is with colleagues in UCL, David Miller in particular. So this study was very simple. We took patients with multiple sclerosis and asked a simple question: Would stem cells from the bone marrow be protective of their nerves? So what we did was we took this bone marrow, grew up the stem cells in the lab, and then injected them back into the vein. I'm making this sound really simple. It took five years off a lot of people, okay? And it put gray hair on me and caused all kinds of issues. But conceptually, it's essentially simple. So we've given them into the vein, right? So in order to measure whether this was successful or not, we measured the optic nerve as our outcome measure. And that's a good thing to measure in M.S., because patients with M.S. sadly suffer with problems with vision -- loss of vision, unclear vision. And so we measured the size of the optic nerve using the scans with David Miller three times -- 12 months, six months, and before the infusion -- and you can see the gently declining red line. And that's telling you that the optic nerve is shrinking, which makes sense, because their nerves are dying. We then gave the stem cell infusion and repeated the measurement twice -- three months and six months -- and to our surprise, almost, the line's gone up. That suggests that the intervention has been protective. I don't think myself that what's happened is that those stem cells have made new myelin or new nerves. What I think they've done is they've promoted the endogenous stem cells, or precursor cells, to do their job, wake up, lay down new myelin. So this is a proof of concept. I'm very excited about that.
Drugi način je da se efikasno spustite u ćelije, da ih presadite, da biste zamenili umiruće ili izgubljene ćelije, čak i u mozgu. Sada ću vam reći o eksperimentu, kliničkom ispitivanju koje smo napravili, nedavno je završeno, sa kolegama na UCL-u, posebno sa Dejvidom Milerom. To je vrlo jednostavna studija. Uzeli smo pacijente s multiplom sklerozom i postavili jednostavno pitanje: Da li bi se matične ćelije iz koštane srži ponašale zaštitnički prema sopstvenim nervima? Tako smo uzeli koštanu srž, uzgojili matične ćelije u laboratoriji, a zatim ih ubrizgali natrag u venu. Čini se kao da je ovo veoma jednostavno. Trajalo je pet godina i puno ljudi, ok? I zbog toga sam osedeo, a izazvalo je svakakve debate. No konceptualno, to je u biti jednostavno. Ubrizgali smo ih u venu. Da bismo izmerili da li je bilo uspešno, merili smo očni nerv kao naš merni rezultat. To je dobra stvar za merenje u MS, jer bolesnici s MS nažalost imaju problema s vidom - gubitak vida, nejasan vid. I tako smo izmerili očni nerv, pomoću snimaka sa Dejvidom Milerom, tri puta - 12 meseci, 6 meseci i pre infuzije - i vidite blago opadanje crvene linije. To govori da se očni nerv skupio, što ima smisla, jer njihovi nervi odumiru. Tada smo dali infuziju matičnih ćelija i ponovili merenje dva puta - za tri i za šest meseci - i na naše iznenađenje, linija je narasla. To sugeriše da je intervencija bila zaštitna. Ne mislim da su te ćelije napravile novi mijelin ili nove nerve. Mislim da su podstakle endogene matične ćelije, odnosno prekursorske ćelije, da rade svoj posao, probude se, polože novi mijelin. Dakle, to je dokaz koncepta. Vrlo sam uzbuđen zbog toga.
So I just want to end with the theme I began on, which was regeneration and hope. So here I've asked John what his hopes are for the future.
Želim još samo da završim temu sa početka svog govora koja je bila regeneracija i nada. Pitao sam Džona čemu se nada u budućnosti.
John: I would hope that sometime in the future through the research that you people are doing, we can come up with a cure so that people like me can lead a normal life.
Džon: Nadam se da će se jednom u budućnosti putem istraživanja koje radite, doći do leka, da bi ljudi kao ja mogli normalno živeti.
SC: I mean, that speaks volumes.
SČ: Mislim da to mnogo govori.
But I'd like to close by first of all thanking John -- thanking John for allowing me to share his insights and these clips with you all. But I'd also like to add to John and to others that my own view is, I'm hopeful for the future. I do believe that the disruptive technologies like stem cells that I've tried to explain to you do offer very real hope. And I do think that the day that we might be able to repair the damaged brain is sooner than we think. Thank you. (Applause)
Završio bih zahvalnicom Džonu - što mi je dozvolio da podelim njegove uvide i ove snimke sa vama. Takođe bih želeo dodati Džonu i drugima da lično gajim nadu za budućnost. Verujem da disruptivne tehnologije poput matičnih ćelija koje sam vam pokušao objasniti nude vrlo realnu nadu. I zaista mislim da će dan kada ćemo moći da popravljamo oštećen mozak doći pre nego što mislimo. Hvala. (Aplauz)