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.
Jako mi je drago što mogu danas ovdje razgovarati s vama o tome kako bi mogli popraviti moždana oštećenja, a posebice sam uzbuđen zbog ovoga, zato što sam neurolog, i vjerujem da ovo nudi jedan od izvrsnih načina kojima bismo mogli pobuditi nadu pacijentima koji danas žive s razarajućim i još neizlječivim 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?
Ovdje leži problem. Možete vidjeti sliku mozga osobe s Alzheimerovom bolešću i zdravi mozak, a očito je da se kod mozga osobe s Alzheimerom, što je zaokruženo crveno, vidi jasno oštećenje – atrofija, ožiljci. Mogao bih vam pokazati jednake slike kod drugih stanja: multiple skleroze, bolesti motoneurona, Parkinsonove ili Huntingtonove bolesti, i sve bi izgledale slično. Zajedno ovi poremećaji mozga predstavljaju jednu od glavnih javnozdravstvenih problema našeg doba. Dobiveni brojevi su prilično zapanjujući. U svakom trenutku postoji 35 milijuna ljudi koji žive s jednim od ovih moždanih poremećaja, a godišnji trošak u globalu iznosi 700 milijardi dolara. Samo razmislite o tome. To je više od jedan posto globalnog BDP-a. Postaje još i gore, zato što ovi brojevi rastu jer je riječ o bolestima naveliko povezanim s godinama, a mi živimo sve duže. Pitanje koje moramo postaviti sami sebi je, zašto, unatoč poražavajućem utjecaju ovih bolesti na pojedinca, izuzev veličine društevnih problema, zašto ne postoje učinkoviti tretmani?
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.
Kako bi ovo razmotrili, prvo vam moram dati brzi tečaj o tome kako mozak funkcionira. Drugim riječima, ispričat ću vam sve što sam naučio na medicinskom fakultetu. (Smijeh) Vjerujte mi, neće trajati predugo. U redu? (Smijeh) Mozak je jako jednostavan: sastoji se od četiri vrste stanica, a dvije su prikazane ovdje. Vidite živčanu stanicu, i mijelinizacijsku stanicu ili izolacijsku stanicu. Ona se zove oligodendrocit. Kada ove četiri stanice rade zajedno u zdravlju i skladu, one stvaraju iznimnu simfoniju električne aktivnosti, a upravo je ta električna aktivnost osnova naše sposobnosti razmišljanja, emotivnosti, sjećanja, učenja, kretanja, osjećanja i drugog. Jednako tako, svaka od ove četiri stanice pojedinačno ili zajedno, može odumrijeti a kada se to dogodi nastaje oštećenje. Nastaje oštećenje veza. Dobijete narušene veze. A to je vidljivo kao sporija provodljivost veza. U konačnici, to oštećenje se očituje kao bolest. Ako je živčana stanica koja umire na primjer, motoneuron, nastat će bolest motoneurona.
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.
Voli bih vam dati primjer iz stvarnog života o onome što se događa kod bolesti motoneurona. Ovo je moj pacijent koji se zove John. Posjetio sam Johna prošli tjedan u bolnici. Zamolio sam ga da nam kaže nešto o svojim problemima koji su doveli do početne dijagnoze bolesti motoneurona.
John: I was diagnosed in October in 2011, and the main problem was a breathing problem, difficulty breathing.
John: Dijagnosticiran sam u studenome 2011, a glavni problem bio je s disanjem, 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.
Siddharthan Chandran: Nisam siguran jeste razumijeli, ali što je John rekao bilo je da su poteškoće s disanjem dovele s vremenom do dijagnoze bolesti motoneurona.
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.
Prošlo je 18 mjeseci od Johnove dijagnoze pa sam ga upitao da nam kaže nešto o 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.
John: Ono što je sada novo je da se disanje pogoršalo. Osjećam slabost u rukama i nogama. Većinu vremena provodim u kolicima.
SC: John's just told us he's in a wheelchair most of the time.
SC: John nam je rekao da je u kolicima većinu 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.
Ono što pokazuju ova dva isječka nisu samo razarajuće posljedice ove bolesti. već nam govore nešto i o šokantnoj dinamici ove bolesti, jer je u samo 18 mjeseci sposobnu odraslu osobu učinila ovisnom o kolicima i respiratoru. Budimo realni, John bi mogao biti nečiji 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.
To se događa kada odumru motoneuroni. Ali što se događa kada propadnu mijelinske stanice? Dobijete multiplu sklerozu. Slika s lijeve strane je ilustracija mozga, to je mapa moždanih veza, koja je prekrivena područjima oštećenja. Nazivamo ih demijeliniziacijskim lezijama. To su oštećenja i bijela 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 sad razmišljate. Mislite: „Moj Bože, ovaj je došao ovdje i rekao da će pričati o nadi, a sve što je ispričao je prilično mračna i depresivna priča.“ Rekao sam vam da su ove bolesti užasne. Razarajuće su, brojevi rastu, cijene su apsurdne, a najgore od svega ne postoji liječenje. Pa gdje je 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.
Znate što? Mislim da postoji nada. I postoji u sljedećem odsječku ove moždane sekcije osobe s multiplom sklerozom, a ono što prikazuje je nevjerojatno, mozak se može popraviti sam. Ali ne čini to dovoljno dobro. I ponovno, postoje dvije stvari koje vam želim pokazati. Prva je oštećenje pacijenta s M.S. To je još jedna od ovih bijelih masa. Ali najbitnije je da crveno zaokruženo područje ističe područje koje je svjetloplavo. Ovo svjetloplavo područje bilo je bijelo. Bilo je oštećeno. A sada je popravljeno. Da pojasnim: To nije zbog liječnika. Već unatoč liječnicima, a ne zbog njih. Ovo je spontani popravak. To je nevjerojatno i dogodilo se jer postoje matične stanice u mozgu koje stvaraju novi mijelin, novu izolaciju koja će biti postavljena oko oštećenih živaca. Ovo opažanje važno je iz dva razloga. Prvi razlog je da osporava jednu od dogmi koje smo naučili na medicini, ili barem ja jesam, priznajem prošlog stoljeća, a to je da se mozak ne može popraviti sam, kao, primjerice, kost ili jetra. Zapravo može, ali ne radi to dovoljno dobro. Druga stvar koju čini a daje nam vrlo jasan smjer traganja za novim terapijama -- ne morate biti posebno inteligentni da znate što učiniti. Potrebno je samo pronaći i način za promicanjem endogenih, spontanih popravaka koji se sami događaju.
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.
Pitanje je, zašto, ako smo to znali neko vrijeme, a jesmo, zašto ne postoji takvo liječenje? A to dijelom odražava složenost razvoja lijekova. Razvoj lijekova možete zamisliti kao prilično skupu i rizičnu okladu, a izgledi za ovu okladu su otprilike ovi: oni su 10,000 naprema 1, zato što je potrebno ispitati oko 10,000 spojeva kako bi se pronašao potencijalni pobjednik. A zatim je potrebno potrošiti 15 godina i oko milijardu dolara, a ni onda, možda nećete imati pobjednika.
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?
Pitanje za nas je, možemo li promijeniti pravila igre i poboljšati izglede? Kako bismo to učinili, treba razmisliti, gdje je napredak u otkrivanju ovog lijeka? Jedan od napredaka nastao je rano u otkrivanju lijeka. Sav taj odabir odnosi se na životinjske modele. A znamo da je pogodno istraživati čovječanstvo na čovjeku, da citiram Alexandera Popea. Pitanje je, možemo li proučavati ove bolesti koristeći ljudski materijal? Naravno da možemo. Možemo koristiti matične stanice, posebice možemo koristiti humane matične stanice. A humane matične stanice su iznimne ali jednostavne stanice koje mogu dvije stvari: imaju sposobnost samoobnove i umnažanja, ali i mogu se sepecijalizirati u koštane, jetrene ili još bitnije živčane stanice, možda čak i motoneurone ili mijelinske stanice. A izazov je dugo bio: možemo li iskoristiti moć, neosporivu moć ovih matičnih stanica s ciljem da ih iskoristimo za regenerativnu neurolgiju?
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.
Ja mislim da možemo, a razlog da možemo je zato što postoji nekoliko velikih otkrića u proteklih 10, 20 godina. Jedno od njih bilo je ovdje u Edinburghu, a to je jedina slavna ovca, Dolly. Dolly je napravljena u Edinburghu, i Dolly je bila primjer prvog sisavca koji je kloniran iz zrelih stanica. Ali mislim da je mnogo značajnije otkriće za potrebne naše današnje rasprave napravio 2006. japanski znanstvanik koji se zvao Yamanaka. Ono što je Yamanaka učinio, u vidu izvrsnog znanstvenog kulinarstva, pokazao je da četiri sastojka, samo četiri sastojka, mogu učinkovito pretvoriti bilo koju stanicu, odraslu stanicu, u glavnu matičnu stanicu. A važnost ovoga teško je preuveličati, zato što to znači da od bilo koga u ovoj prostoriji, a osobito bolesnika, sada možete stvoriti po mjeri, osoban set za popravak tkiva. Uzmete stanicu kože, učinite ju pluripotentnom stanicom, kako bi mogle napraviti one stanice koje su bitne za neku bolest, za proučavanje, ali i potencijalno liječenje. Ta ideja na medicinskom fakultetu -- ova se tema ponavlja, zar ne, medicinski fakultet i ja? — bila bi smiješna, ali je danas stvarnost. Gledam na ovo kao temelj za regeneraciju, popravak i nadu.
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 kad smo već na temi nade za vas koji možda niste imali uspjeha u školi, postoji nada i za vas, zato što je ovo školsko izvješće Johna Gerdona. [„Mislim da ima želju postati znanstvenik; kako se dosad pokazao to je poprilično smiješno.“] Nisu tada imali visoko mišljenje o njemu. Ali ono što možda ne znate je da je dobio Nobelovu nagradu za medicinu prije tri mjeseca.
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.
Da se vratim prvotnom problemu, koja je mogućnost da ove matične stanice, ili ova disruptivna tehnika, poprave oštećeni mozak, a zovemu ju regenerativna neurologija? Mislim da postoje dva načina razmišljanja o ovome: kao fanatastičan ljekoviti izum 21. stoljeća I/ili kao oblik terapije. Želim vam reći nešto o oba u sljedećim trenucima.
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.
Ljudi često pričaju o ovome kao lijek otkriven u posudici. Vrlo je jednostavno: Uzmete pacijenta sa bolešću, primjerice motoneurona, uzmete uzorak kože, napravite pluripotentno reprogramiranje, kao što sam prije rekao, i uzgajate živu motornu živčanu stanicu. To je pojednostavljeno, zato što je to ono što pluripotentne stanice mogu. Bitno je da možete usporediti njihovo ponašanje s njima jednakim, ali zdravim parom, idealno, od zdravog rođaka. Na taj način, odgovarajuće su za genetske varijacije.
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.
A to je upravo ono što smo učinili ovdje. Ovo je bilo u suradnji s kolegama: iz Londona, Chris Shaw, iz SAD-a, Steve Finkerbeiner i Tom Maniatis. Ono što gledate vrlo je nevjerojatno, to su živi, rastući, motoneuroni od pacijetna s bolesti motoneurona. U ovom slučaju naslijeđeni oblik. Samo zamislite ovo. To je bilo nezamislivo prije 10 godina. Osim što ih vidimo kako rastu i rade različite procese možemo ih učiniti flourescentnima a što je bitno, tada možemo pratiti zdravlje svake posebno te usporediti boelsne motoneurone sa zdravima. A kada to učinite i stavite ih zajedno, uočavamo da one bolesne, koje su predstavljene crvenom linijom, imaju dva i pol puta veću vjerojatnost da umru od zdravog para. Bitna stvar u ovome je da onda imate odličan testa za otkrivanje lijekova, zato što ono što bi tražili od lijeka, a to možete učinit pomoću visoko-protočni automatizirani probirni sustav, zatražili biste od lijeka jednu stvar: pronađi mi lijek koji će crvenu liniju dovesti bliže plavoj liniji zato što će taj lijek tada biti kandidat visoke vrijednosti koji bi vjerojatno mogli odnijeti na ljudsko ispitivanje i gotovo zaobići to usko grlo o kojem sam vam pričao kod otkrivanja lijekova na životinjskim modelima, ako to ima smisla. To je odlično.
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 želio bih se vratiti na to kako bi mogli koristiti matične stanice izravno za popravak oštećenja. Opet postoje dva načina razmišljanja o ovome, i međusobno se ne isključuju. Prvi, a mislim i na duge staze onaj koji će nam dati najveće dividende, ali se o njemu još ne razmišlja na taj način, je da razmislimo o matičnim stanicama koje su već u našem mozgu, a to sam vam rekao. Svi imamo matične stanice u mozgu, čak i u bolesnom mozgu, a sigurno pametan put za napredak je pronaći načine kako potaknuti i aktivirati te matične stanicu koje su već u mozgu da na odgovarajući reagiraju i odgovore na štetu i poprave ju. To je budućnost. Postojat će lijekovi koji će to moći 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 učinkovito uzmu stanice, transplantiraju da zamjene umiruće ili izgubljene stanice, čak i u mozgu, Želim vam reći za eksperiment, kliničko ispitivanje koji smo napravili koje je nedavno dovršeno, sa kolegama s UCL-a, posebice Davidom Millerom. Ispitivanje je bilo vrlo jednostavno. Izabrali smo pacijente s multiplom sklerozom i pitali jednostavno pitanje: Bi li matične stanice iz koštane srži štitile svoje živce? Ono što smo napravili je da smo uzeli koštanu srž, uzgojili matičnu stanicu u laboratoriju, a zatim je ubrizgali natrag u venu. Čini vam ovo vrlo jednostavnim. Oduzelo je pet godina mnogim ljudima, u redu? A mene je posijedilo i uzrokovalo razne probleme. No konceptualno je vrlo jednostavno. Ubacili smo ih natrag u venu, zar ne? Kako bi izmjerili je li ovo bilo uspješno ili ne, uzeli smo vidni živac kao ishod mjerenja. A to je dobra stvar za mjeriti u M.S. jer bolesnici s M.S. nažalost pate od problema s vidom -- gubitak vida, nejasan vid. Mjerili smo veličinu vidni živca s Davidom Millerom koristeći skenere tri puta -- 12 mjeseci, šest mjeseci i prije infuzije -- i možete vidjeti lagano padanje crvene linije. A to vam govori da se vidni živac smanjuje, što ima smisla, jer odumiru njegovi neuroni. zatim smo dali infuziju matičnih stanica i ponovili mjerenje dva puta -- tri mjeseca i šest mjeseci -- i na naše iznenađenje, linija je porasla. To upućuje da je intervencija bila preventivna. Ne mislim da je ono što se dogodilo da su matične stanice napravile novi mijelin ili nove neurone. Ono što ja mislim je da su potaknule endogene matične stanice ili prekursorske stanice, na posao, probudile ih da stvaraju novi mijelin. Ovo je dokaz ideje. Jako 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 završiti s temom s kojom sam započeo, a to je regeneracija i nada. Upitao sam Johna koja su njegova nadanja za budućnost.
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.
John: Nadam se da će jednom u budućnosti kroz istraživanja koja vi ljudi radite, proizvesti lijek kako bi ljudi kao ja mogli voditi normalan život.
SC: I mean, that speaks volumes.
To dovoljno 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)
Želio bih završiti prije svega zahvalivši Johnu -- zahvalan sam što je dopustio da podijelim njegov uvid i ove isječke s vama svima. Htio bih dodati za Johna i ostale da sam osobno pun nade za budućnost. Vjerujem da će disruptivne tehnologije kao matične stanice koje sam pokušao objasniti pružaju stvarnu nadu. Mislim da će dan kada ćemo biti u mogućnosti popravljati moždana oštećenja doći ranije nego što mislimo. Hvala. (Pljesak)