TED 테드로 영어공부 하기 What you can do to prevent Alzheimer by Lisa Genova

 

안녕하세요, Davey 입니다. 요즘에는 정말 깜박 깜박하는 거 같습니다. 하고 싶은건 많은데, 시간은 부족한거 같고, 그러면서, 약간 늦게 일어나기도 하고, 빨리 일어나면, 잠이 부족해서 힘들고, 정말 양날의 칼인거 같습니다. 자기전에 자기한테 주는 선물이라고, 약간의 동영상을 보는데, 그것도 좀 줄여야 겠습니다. 머, 이렇게 깜박 깜박하는 현상과 관련된 speech 를 오늘 posting 하려고 합니다. Title은 What you can do to prevent Alzheimer's 은 입니다. 아래 Link 를 통해서, TED Talk 들으실 수 있습니다.

 

https://www.ted.com/talks/lisa_genova_what_you_can_do_to_prevent_alzheimer_s

What you can do to prevent Alzheimer's

 

일단, 첫 문장은, 80세까지 살고 싶은 사람이 얼마나 있을까요? 라고 질문을 던집니다. 모두 다 오래 살고 싶을 겁니다. 하지만 건강하게요! 무튼, 그렇게 질문을 던지고, 미래 우리가 85세 됐을 때를 상상해보고, 그때 둘중에 하나는 알츠하이머에 걸렸을거라는 거라고 합니다. 다들 같은 마음일겁니다.

 

 나는 아닐거라고. 그리고 나서, 알츠하이머가 왜 걸리고, 어떤 과정을 통해서, 머리의 건강이 악화되는지를 설명을 합니다. 간단히 설명하면, 뉴론이라는 신경 세포를 연결해주고, 정보를 전달해주는 역할을 하는 신경줄기, 소위 synapse 가 있는데, 그 synapse가 손상이 되고, 그 부분에, 아밀로이드 베타가 축적되면서, 아밀로이드 반 이라는 단백질 비축물의 축적으로 인해, 신경 세포가 파괴되고, 더이상 정보를 교환하고 뉴론 사이의 활동을 활성하지 하지 못함으로서, 알츠하이머가 생긴다고 합니다. 즉, 우리의 기억 능력이 점점 저하 된다는 겁니다.

 

 40세나 40세 이상이되면, 이 아밀로이드 베타의 축적이 시작이 되고, 10~20년이 지나면 많은 양이 축적이 될 거라고 설명을 이어 갑니다. 하지만, 나쁜애기만 하는건 아니네요! 이렇게 축적이 이뤄지지는 걸 천천히 하고, 축적이 되더라도 알츠하이머에 안걸리는 방법을 애기해줍니다. 이론은 단순합니다. 새로운 것을 배우면 그 축적을 막을 수 있다는 거죠. 그리고, 아밀로이드 베타의 축적으로 인해 파괴된 synapse가 있다고 하더라도, 다른 여러가지의 synapse를 가지고 있다면, 기억력의 능력은 약간은 쇠퇴하겠지만, 알츠하이머처럼, 기억력의 급격한 저하는 이뤄지지 않을 거라는 거죠. 언어 공부도 알츠하이머 안걸리는 한가지의 방법이라고 하네요^^

 

 우리 모두 다들 좋은 거 하는 거라고 생각하고 더 열심히 하시죠. 그리고 마지막으로 알츠하이머라고 진단을 걸렸더라도, 너무 절망하지 말라는 거죠. 진단은 진단이고, 우리는 계속적으로 살아갈거라고, 그러니까, 힘내자 이런 느낌으로 이해했습니다. 맞는 애기인거 같습니다. 힘든일이 있더라도, 절망하지 말고, 더 열심히 살아가면 언제가는 기회가 아니면 더 좋은 시간이 있지 않을까 합니다. 그럼 설명은 여기까지만하고, 아래 script & word 참조해서, 열공합시다! 아래 script는 TED 홈페이지 해당 speech의 Transcript 내용 참조하였습니다.

 

- What you can do to prevent Alzheimer's script & words

 

TED 영상 사진 참조

 

How many people here would like to live to be at least 80 years old? Yeah. I think we all have this hopeful expectation of living into old age. Let's project out into the future, to your future "you's," and let's imagine that we're all 85. Now, everyone look at two people. One of you probably has Alzheimer's disease.
 

project out 미래를 투영하다, 상상하다, 생각하다

(Laughter)
 
Alright, alright. And maybe you're thinking, "Well, it won't be me." Then, OK. You are a caregiver. So
 

caregiver 돌보는 사람

 

(Laughter)
 
so in some way, this terrifying disease is likely to affect us all.
 
Part of the fear around Alzheimer's stems from the sense that there's nothing we can do about it. Despite decades of research, we still have no disease-modifying treatment and no cure. So if we're lucky enough to live long enough, Alzheimer's appears to be our brain's destiny.
 

stem 줄기, 막다, 저지하다 

But maybe it doesn't have to be. What if I told you we could change these statistics, literally change our brain's destiny, without relying on a cure or advancements in medicine?
 
Let's begin by looking at what we currently understand about the neuroscience of Alzheimer's. Here's a picture of two neurons connecting. The point of connection, this space circled in red, is called the synapse. The synapse is where neurotransmitters are released. This is where signals are transmitted, where communication happens. This is where we think, feel, see, hear, desire ... and remember. And the synapse is where Alzheimer's happens.
 
Let's zoom in on the synapse and look at a cartoon representation of what's going on. During the business of communicating information, in addition to releasing neurotransmitters like glutamate into the synapse, neurons also release a small peptide called amyloid beta. Normally, amyloid beta is cleared away metabolized by microglia, the janitor cells of our brains. While the molecular causes of Alzheimer's are still debated, most neuroscientists believe that the disease begins when amyloid beta begins to accumulate. Too much is released, or not enough is cleared away, and the synapse begins to pile up with amyloid beta. And when this happens, it binds to itself, forming sticky aggregates called amyloid plaques.

 

cartoon representation 만화 설명

glutamate 글구탄사염

peptide 펩티드 아미노사 화합물

amyloid beta 아밀로이드 베타

molecular 분자된, 분자의

metabolized by microglia 소교세포로 대사된

janitor cells 관리 세포

aggregate 집합체

amyloid plaque 아밀로이드 반 

 

 

How many people here are 40 years old or older? You're afraid to admit it now. This initial step into the disease, this presence of amyloid plaques accumulating, can already be found in your brains. The only way we could be sure of this would be through a PET scan, because at this point, you are blissfully unaware. You're not showing any impairments in memory, language, or cognition ... yet. We think it takes at least 15 to 20 years of amyloid plaque accumulation before it reaches a tipping point, then triggering a molecular cascade that causes the clinical symptoms of the disease. Prior to the tipping point, your lapses in memory might include things like, "Why did I come in this room?" or "Oh ... what's his name?" or "Where did I put my keys?"
 

blissfully 행복에 넘쳐서

impairment 해침, 손상, 장애

your lapses 쇠퇴, 전락

 

Now, before you all start freaking out again, because I know half of you did at least one of those in the last 24 hours -- these are all normal kinds of forgetting. In fact, I would argue that these examples might not even involve your memory, because you didn't pay attention to where you put your keys in the first place. After the tipping point, the glitches in memory, language and cognition are different. Instead of eventually finding your keys in your coat pocket or on the table by the door, you find them in the refrigerator, or you find them and you think, "What are these for?"
 

glitche 작은 결함, 작은 기술상의 문제

So what happens when amyloid plaques accumulate to this tipping point? Our microglia janitor cells become hyper-activated, releasing chemicals that cause inflammation and cellular damage. We think they might actually start clearing away the synapses themselves. A crucial neural transport protein called "tau" becomes hyperphosphorylated and twists itself into something called "tangles," which choke off the neurons from the inside. By mid-stage Alzheimer's, we have massive inflammation and tangles and all-out war at the synapse and cell death.

 

inflammation 연소 염증 불타기

tangle 얽힌 것

all-out war 총력전

So if you were a scientist trying to cure this disease, at what point would you ideally want to intervene? Many scientists are betting big on the simplest solution: keep amyloid plaques from reaching that tipping point, which means that drug discovery is largely focused on developing a compound that will prevent, eliminate, or reduce amyloid plaque accumulation. So the cure for Alzheimer's will likely be a preventative medicine. We're going to have to take this pill before we reach that tipping point, before the cascade is triggered, before we start leaving our keys in the refrigerator. We think this is why, to date, these kinds of drugs have failed in clinical trials -- not because the science wasn't sound, but because the people in these trials were already symptomatic. It was too late. Think of amyloid plaques as a lit match. At the tipping point, the match sets fire to the forest. Once the forest is ablaze, it doesn't do any good to blow out the match. You have to blow out the match before the forest catches fire.

 

intervene 개입하다 끼어들다

symptomatic 징후가 나타나는, 전조가 나타나는

a lit match 불붙은 성냥

 
Even before scientists sort this out, this information is actually really good news for us, because it turns out that the way we live can influence the accumulation of amyloid plaques. And so there are things we can do to keep us from reaching that tipping point.
 
Let's picture your risk of Alzheimer's as a see-saw scale. We're going to pile risk factors on one arm, and when that arm hits the floor, you are symptomatic and diagnosed with Alzheimer's. Let's imagine you're 50 years old. You're not a spring chicken anymore, so you've accumulated some amyloid plaques with age. Your scale is tipped a little bit.
 
Now let's look at your DNA. We've all inherited our genes from our moms and our dads. Some of these genes will increase our risk and some will decrease it. If you're like Alice in "Still Alice," you've inherited a rare genetic mutation that cranks out amyloid beta, and this alone will tip your scale arm to the ground. But for most of us, the genes we inherit will only tip the arm a bit. For example, APOE4 is a gene variant that increases amyloid, but you can inherit a copy of APOE4 from mom and dad and still never get Alzheimer's, which means that for most of us, our DNA alone does not determine whether we get Alzheimer's. So what does? We can't do anything about getting older or the genes we've inherited. So far, we haven't changed our brain's destiny.
 
What about sleep? In slow-wave deep sleep, our glial cells rinse cerebral spinal fluid throughout our brains, clearing away metabolic waste that accumulated in our synapses while we were awake. Deep sleep is like a power cleanse for the brain. But what happens if you shortchange yourself on sleep? Many scientists believe that poor sleep hygiene might actually be a predictor of Alzheimer's. A single night of sleep deprivation leads to an increase in amyloid beta. And amyloid accumulation has been shown to disrupt sleep, which in turn causes more amyloid to accumulate. And so now we have this positive feedback loop that's going to accelerate the tipping of that scale.
 

ablaze 타서, 흥분하여, 타올라서

glial cell 아교세포

cerebral 뇌의 대뇌의

spinal fluid 척수액

metabolic wast 신진대사의 노폐물

hygiene 위생, 건강법

 

 

What else? Cardiovascular health. High blood pressure, diabetes, obesity, smoking, high cholesterol, have all been shown to increase our risk of developing Alzheimer's. Some autopsy studies have shown that as many as 80 percent of people with Alzheimer's also had cardiovascular disease. Aerobic exercise has been shown in many studies to decrease amyloid beta in animal models of the disease. So a heart-healthy Mediterranean lifestyle and diet can help to counter the tipping of this scale.
 

cardiovascular 심장혈관의

diabetes 당뇨병

autopsy 부검

mediterranean 지중해의

 

So there are many things we can do to prevent or delay the onset of Alzheimer's. But let's say you haven't done any of them. Let's say you're 65; there's Alzheimer's in your family, so you've likely inherited a gene or two that tips your scale arm a bit; you've been burning the candle at both ends for years; you love bacon; and you don't run unless someone's chasing you.
(Laughter)
 
Let's imagine that your amyloid plaques have reached that tipping point. Your scale arm has crashed to the floor. You've tripped the cascade, setting fire to the forest, causing inflammation, tangles, and cell death. You should be symptomatic for Alzheimer's. You should be having trouble finding words and keys and remembering what I said at the beginning of this talk. But you might not be.
 
There's one more thing you can do to protect yourself from experiencing the symptoms of Alzheimer's, even if you have the full-blown disease pathology ablaze in your brain. It has to do with neural plasticity and cognitive reserve. Remember, the experience of having Alzheimer's is ultimately a result of losing synapses. The average brain has over a hundred trillion synapses, which is fantastic; we've got a lot to work with. And this isn't a static number. We gain and lose synapses all the time, through a process called neural plasticity. Every time we learn something new, we are creating and strengthening new neural connections, new synapses.
 

full-blown 성숙한

 

In the Nun Study, 678 nuns, all over the age of 75 when the study began, were followed for more than two decades. They were regularly given physical checkups and cognitive tests, and when they died, their brains were all donated for autopsy. In some of these brains, scientists discovered something surprising. Despite the presence of plaques and tangles and brain shrinkage -- what appeared to be unquestionable Alzheimer's -- the nuns who had belonged to these brains showed no signs of having the disease while they were alive.
 
How can this be? We think it's because these nuns had a high level of cognitive reserve, which is a way of saying that they had more functional synapses. People who have more years of formal education, who have a high degree of literacy, who engage regularly in mentally stimulating activities, all have more cognitive reserve. They have an abundance and a redundancy in neural connections. So even if they have a disease like Alzheimer's compromising some of their synapses, they've got many extra backup connections, and this buffers them from noticing that anything is amiss.
 

pathology 병리학

plasticity 유연성, 적응성

cognitive reserve 인지능력

literacy 읽고 쓰는 능력

abundance 풍부 다량

compromising 손상시키다

buffer 완화하다

amiss 부적당하게, 적절하지 않아

 

 

Let's imagine a simplified example. Let's say you only know one thing about a subject. Let's say it's about me. You know that Lisa Genova wrote "Still Alice," and that's the only thing you know about me. You have that single neural connection, that one synapse. Now imagine you have Alzheimer's. You have plaques and tangles and inflammation and microglia devouring that synapse. Now when someone asks you, "Hey, who wrote 'Still Alice?'" you can't remember, because that synapse is either failing or gone. You've forgotten me forever.
 
But what if you had learned more about me? Let's say you learned four things about me. Now imagine you have Alzheimer's, and three of those synapses are damaged or destroyed. You still have a way to detour the wreckage. You can still remember my name. So we can be resilient to the presence of Alzheimer's pathology through the recruitment of yet-undamaged pathways. And we create these pathways, this cognitive reserve, by learning new things. Ideally, we want these new things to be as rich in meaning as possible, recruiting sight and sound and associations and emotion.
 

wreckage 난파, 파멸, 잔해

recruitment 회복

rich in meaning 의미상으로 풍부한 , 의미심장한

So this really doesn't mean doing crossword puzzles. You don't want to simply retrieve information you've already learned, because this is like traveling down old, familiar streets, cruising neighborhoods you already know. You want to pave new neural roads. Building an Alzheimer's-resistant brain means learning to speak Italian, meeting new friends, reading a book, or listening to a great TED Talk.
 
And if, despite all of this, you are someday diagnosed with Alzheimer's, there are three lessons I've learned from my grandmother and the dozens of people I've come to know living with this disease. Diagnosis doesn't mean you're dying tomorrow. Keep living. You won't lose your emotional memory. You'll still be able to understand love and joy. You might not remember what I said five minutes ago, but you'll remember how I made you feel. And you are more than what you can remember.
 
Thank you.
 
(Applause)
 

언어공부하면서 저희도, 알츠하이머 안걸리게 조심합시다. 감사합니다.

 

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