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.
今天我感到非常開心來這裡, 要跟你們大家談: 「如何我們有可能修復 受損的大腦」 這方面使我特別地感到振奮, 因為我身為一個神經學專家, 我相信這提供了 一個最棒的辦法, 讓我們也許有能力送上希望 給病人們, 那些今天活著帶有造成損傷、 尚未能治癒的大腦病變的人。
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?
問題就在這裡, 你可以看到這是某人大腦的圖片, 是患有阿滋海默症的人。 旁邊還有健康的大腦圖片, 很明顯的是在患有 阿滋海默症的大腦中 被紅線圈起來的是明顯的損傷--- 萎縮和傷疤。 我還可以讓你看更多同性質的照片, 來自其他大腦病變:多發性硬化症、 運動神經疾病、巴金森氏症、 甚至還有亨丁頓氏症, 而且它們都訴說著相似的故事, 還有這些大腦失常集合性地代表 我們此生主要的一個公眾健康威脅。 況且這人數真的讓人傻眼, 以今天而言有三千五百萬人, 患有這些病變的其中一種, 而且年度的花費全球性來說 是七千億美金。 就單單想一下那個金額, 那是遠大於百分之1 的全球國內生產毛額。 而且還會變糟, 因為人數、花費等所有的數據 一直在上升中, 因為這些絕大部分是 年齡相關疾病而我們正活得更長壽。 所以我們真正需要問我們自己的問題是 什麼原因使得破壞性影響的 這些大腦病變 發生在個人身上? 先不要關心到後續 造成的社會問題的規模。 為什麼沒有能成功的療法?
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.
現在為了要認真思考這問題, 我必須先給你們上一堂速成課, 有關大腦是如何運作。 所以換句話說我必須告訴你們 我在醫學院裡學到的所有一切。 (笑聲) 不過相信我! 這預計不會花太久, 可以吧? 大腦組織真的再簡單不過, 它是由四種細胞組成的, 這邊展示了其中的兩種, 有神經細胞、 再來是髓鞘細胞, 或叫絕緣細胞。 這叫寡突膠細胞。 當四種細胞一起運作, 是在健康跟和諧之下, 它們像電流般的傳輸行為 譜了出色的交響曲, 而且正是這些像電流般 的傳輸行為, 支持我們去思考、表達情緒、 記住、學習、移動、 感知等等的能力。 但同等地每一個這四種細胞 單獨或一起可能不受控制或者死掉, 當這情況發生時你就會受到傷害, 你會發生大腦網絡損壞、 你會發生大腦連結中斷, 這邊就是證據, 有著較慢的大腦傳輸。 最終這種損壞將肯定地表示 是大腦病變。 如果最先開始死掉的神經細胞, 例如是運動神經細胞 你就會有運動神經細胞病變。
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.
因此,我想要給你們 看一個真人實例, 患有運動神經細胞病變 會有甚麼事發生? 這位是我的一位病人叫約翰 我才在上個星期的門診看過約翰, 我請約翰來告訴我們 有關他當時有甚麼毛病, 造成之後首次診斷 是運動神經細胞病變。
John: I was diagnosed in October in 2011, and the main problem was a breathing problem, difficulty breathing.
我在2011年十月時就診的, (吃力呼吸) 當時主要的問題是有關呼吸方面, 呼吸困難。
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.
我不知道你是否全部聽清楚了, 約翰想告訴我們 是呼吸的時候會有困難, 導致最後的診斷出 運動神經細胞病變。
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.
約翰從那次診斷到現在 已過了18個月, 我現在請他來告訴我們關於 他目前的困境。
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.
我現在變得呼吸更吃力、 我的手、上肢、下肢變得無力, 所以基本上我大部分時間都 坐在輪椅裡。
SC: John's just told us he's in a wheelchair most of the time.
約翰告訴我們他是坐著輪椅 在大部分時間裡。
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.
所以這兩段短片所要表達的 不只是有關大腦病變的 嚴重傷害性的後果, 而它們也告訴我們有關 病變驚人的惡化速度, 因為只是在18個月之內, 一個健全的成年男人已經給送上 了輪椅而且要依靠呼吸器。 讓我們正視它, 約翰有可能是任何人的父親、 兄弟或朋友。
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.
這就是當運動神經細胞 死亡時會發生的事。 那髓鞘細胞死亡時又會如何? 你將患有多發性硬化症。 所以在你左手邊的掃描 正是一張大腦的圖片, 而且它也是大腦連結路徑的地圖, 上面又被標記出的是 大腦受損的地方, 我們稱作「去髓鞘損傷」, 不過它們壞掉了、還有是白色的。
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?
我知道你在想什麼, 你正在想,「我的天哪! 這傢伙上台來, 說他想談的是希望, 所有他做的事就是說了再無望不過 以及令人沮喪的故事。」 我剛跟你說過這些病變是可怕的。 它們是傷害性的、數字一直上升中的、 費用是太離譜的,且最糟糕的是 我們沒有治療方法,希望在哪裡呢?
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.
你們知道嗎我認為是有希望的, 而且希望就在旁邊那張剖面圖裡, 是某位患有多發性硬化症病人 的大腦剖面圖, 因為令人驚訝地是它說明了, 大腦能夠自癒, 它只是自癒做得還不夠好。 有兩件事我要告訴你。 首先,是患有多發性硬化症的 這個病人大腦有損傷。 再來一次就是這些白色區塊的一塊。 但很重要地,是這個被紅色圈起來的地方 註記了一個淡藍色的區域, 但是那個淡藍色的區域原本是白色的。 就是說它曾經是受損的, 現在已經修復了。 再澄清一些,這不是醫生們造成的。 這是醫生以外的因素, 不是醫生們造成的。 這是自主性的修復。 這很令人驚奇的而且它發生了 就是因為大腦中有幹細胞, 甚至可以使新的髓鞘細胞、絕緣體 包覆在受損的神經上。 這個觀察之所以重要有兩個原因, 第一、是它質疑了一個正統學說 就是我們當初在醫學院裡學到的, 起碼是我曾學習到, 誠然地是在上個世紀時, 就是大腦不能自癒, 不像好比說是骨頭或肝臟。 不過實際上它可以自癒, 只是它自癒得還不夠好。 它做的第二件事, 它給了我們一個清楚的方向 去找出新的療法, 我說的是你不必是極聰明的人, 去知道這裡要做甚麼。 你僅需要找出方法來促使 內生性、自主性的修復 無論如何都能啟動。
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.
問題是如果我們已經知道這些 有一段時間了, 為什麼我們還沒有治療那 些大腦損傷的方法? 那有一部分原因反映出藥品開發 的複雜性。 現在藥品開發你可能會想到 既昂貴又有風險的賭博, 而這賭博的實現機率大概是 萬分之一, 因為你需要測試約ㄧ萬種配方, 去找出那一個有可能成功的正解。 接著你需要花15年的時間, 以及支出超過10億美元, 甚至到後來你並沒有正解。
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?
所以我們該問的問題是, 你可以改變遊戲規則嗎? 你可以縮短找到正解的時間嗎? 為了達到這個目的你必須去想, 藥品開發的瓶頸在哪? 其中一個瓶頸在藥品開發的初期, 所有的測試都發生在動物實驗體上。 不過我們知道 正確的研究人類要用真人, 我借用亞歷山大.波普的話。 所以問題是:我們能否研究這些疾病 使用真人? 當然,我們絕對可以。 我們可以用幹細胞, 尤其是人類的幹細胞, 人類的幹細胞是很不一樣 但又簡單的細胞,可以做到兩件事情: 它們懂得再生 或是製造出更多幹細胞, 它們可以特化為 骨頭、肝臟,或者很關鍵地 -神經的細胞, 可能甚至是運動神經細胞, 或是髓鞘細胞。 而存在了很久的挑戰是 我們是否能獲取這份力量, 這些幹細胞無庸置疑的力量, 來實現它們為 再生神經學帶來的好消息?
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.
我想我們現在可以, 而我們可以的理由 是因為在過去的10~20年間 有很多重大的發現。 其中之一就發生在愛丁堡這裡, 而牠必定是唯一的名羊 ~桃麗。 桃麗是在愛丁堡製造的, 桃麗也是一個例子 第一個複製哺乳類 取樣自成羊細胞。 但我認為更重大的突破, 與我們今天的討論目的相關的 是2006年由一位 日本的科學家做出的, 是山中伸彌 (Yamanaka) 。 而山中伸彌所做的, 在一個神奇的科學大熔爐, 是他指出四種成分, 只要四種成分, 能夠成功地轉換任何細胞、成人細胞 成為主要的幹細胞。 而這個突破的重大性 高到不能再誇大, 因為它表示從在這房間的每個人 特別是病人, 你可以產生 客製化、個人化的細胞修復包。 取下皮膚細胞把它變成 主要的多功能幹細胞, 接著你可以用那些細胞, 與大腦病變有關連的細胞 既可用於研究,又可用於治療。 這個想法在醫學院 不是一直不斷上演的主題嗎? 對我和醫學院而言 可以說是再荒唐不過的。 但在今天它絕對是事實。 我則把它視為 重建、修復與希望的基礎。
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.
既然我們在談"希望"這個主題, 對你們也許曾在學校被當掉的人而言, 你們一樣是有希望的。 因為這是約翰.格登的成績報告書: 「我相信他有想要成為科學家這想法; 以他現在的表現來說是相當荒謬的。」 所以他們之後並不常想起他, 不過你可能不知道 他得了諾貝爾醫學獎 就在三個月之前。
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.
讓我們回到原來的問題, 這些幹細胞成功的機會在哪裡? 或者這顛覆性性科學 用來療癒受損的大腦, 我們現在稱做重建神經學。 我認為你有兩個方向來看它: 當它是神奇的21世紀藥品開發的工具 或者是一種治療手段。 我想再多告訴你一些有關這兩者的事 就在接下來的幾分鐘,
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.
在培養皿裡做藥品研究是人們 最常想到的, 這很簡單,你找一位病人 假定是患有運動神經疾病, 你做一個皮膚的取樣, 你把它重編為多功能幹細胞, 就像我已經跟你說過的, 你可以產生活的運動神經元細胞。 就是這麼直接,因為那就是 多功能幹細胞可以做到的事。 但很重要地,你可以把它們的活動 與相同的但健康的原生細胞作比較, 理想上是與未受到影響的 周邊細胞相比, 這麼做你就吻合了基因的差異性。
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.
這正是我們這裡一直以來在做的事。 這是同事們之間共同合作的成果, 有在倫敦的克力斯.修、 美國的史蒂夫.芬博納、 湯姆.曼尼亞提斯。 而你正看著的圖片是非常讓人驚訝的, 這些是活的、一直在成長的 運動神經細胞, 來自一個患運動神經疾病的病人。 它是遺傳造成的, 就想像看看, 這在十年前可還無法想像的。 除了看著它們成長 以及死亡的過程之外, 我們還可以設計讓它們發出螢光, 但很重要地,我們能因此追蹤 它們各自的健康 用來比較不健康的運動神經細胞 和健康的(運動神經)細胞。 當你做這些事 以及把結果擺在一起時, 你會明白不健康的細胞, 被紅線代表的這邊, 是2又1/2倍的機率會死 與健康的對照細胞相比。 重點是你之後會有 非常棒的鑑定方法來找出藥品, 因為你想知道有關藥品的事情, 你就可以經由大量看完 自動播放影片系統。 你只要藥物幫你做一件事: 幫你找到一種藥可以帶紅線 更靠近藍線, 因為那種藥將會是 有高度價值的候選者, 讓你可以高度可能地直接做人體試驗, 幾乎可以越過瓶頸, 也就是我剛跟你說會在藥物發明 用動物實驗體的不足, 如果這有道理,會是非常棒的。
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.
但我想回到 如何讓你能直接使用幹細胞 來修復損傷。 一樣的有兩個方向來思考這件事, 它們不是完全不相容的。 第一、我想長遠來看 這會給我們最大的好處, 而且還沒有其他人這樣想過, 是去思考那些已經在你 大腦中的幹細胞 就像我剛跟你說的那樣。 我們所有人的大腦都有幹細胞, 甚至在發生病變的大腦, 當然往前進的聰明的方法是 找到讓你可以促進與活化 這些已經在你大腦裡的幹細胞, 適當地對損傷做反應、回應, 來修復它。 這會是未來的前景。 將會有藥物能夠做這件事。
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.
而另外一個想法是 有效地空投進細胞, 把它們移植進去, 以取代正在死亡或逝去的細胞, 甚至是大腦裡面。 我現在要告訴你一個實驗, 是一個我們做過的臨床試驗, 最近才剛做完的, 與我們在倫敦大學學院的同事們, 尤其是大衛.米勒。 這研究很簡單, 我們找來了患有多發性硬化症的病人們, 想一個簡單的問題, 會否從骨髓中取出的幹細胞, 對他們的神經細胞是有保護的? 所以我們所做的是從取出骨髓, 在實驗室裡培養幹細胞, 再把它們重新注入靜脈。 我試著讓這聽起來非常簡單, 這花我們五年的時間、很多人力,知道嗎? 它也讓我有了灰頭髮, 也引起了各種問題。 但概念上而言它是基礎地簡單。 所以我們已經把它們送進靜脈,對吧? 為了評量到底這個手段成不成功, 我們評量視神經, 作為我們的評量結果。 對要來評量多發性硬化症病人 也是一件好事 因為患有多發性硬化症的病人不幸地遭受 與視力有關的問題, 如失明、看不清楚, 所以我們評量視神經的大小 與大衛.米勒一起用掃描器 三遍:12個月前、6個月前、 以及注射之前。 你可以看到那稍微降低的紅線。 那是要告知你視神經正在萎縮中, 那講得通的,因為他們的 神經細胞正在死亡中。 接著我們做了幹細胞注射, 又做了兩次評量, 3個月後和6個月後, 讓我們大部分人驚訝的是 那條紅線往上爬升了。 這表明了介入注射 是有保護性的, 我個人不認為 是因為那些幹細胞 製造出新的髓鞘細胞, 或是新的神經細胞, 我認為它們做到的是它們促使 了內生性的幹細胞或者前身細胞 去做它們的工作, 醒來、覆蓋上新的髓鞘, 這是一個有證據的想法, 我可是對這感到興奮的。
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.
所以我就想要用 我剛開始談的主題做結束, 也就是再生與希望。 我也問過了約翰 他對未來有什麼希望?
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.
我會希望 在未來的某個時點 經由你們現在在做的研究 我們能找出解藥, 然後和我一樣的人 能夠過正常的生活。
SC: I mean, that speaks volumes.
我想,這很明確。
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)
不過我想先謝謝約翰來作結尾, 謝謝約翰同意我來分享 他的想法和這些短片給你們大家。 但我還想要做補充給約翰和其他人, 我個人的觀點是 我對未來是有希望的。 我相信這些顛覆性的科技 像是我試著解釋 給你們聽的幹細胞 的確帶來希望。 我認為那一天, 我們可能有能力 修復受損的大腦的那天, 是比我們想像的來得快。 謝謝。 (掌聲)