How many people here would like to live to be at least 80 years old?

在場有多少人 希望能活到 80 歲以上？

I think we all have this hopeful expectation

and let&#39;s imagine that we&#39;re all 85.

想像我們現在全都已變成 85 歲。

現在，每個人分別看向兩個人，

One of you probably has Alzheimer&#39;s disease.

你們之中其中一個 可能就有阿茲海默症。

And maybe you&#39;re thinking, "Well, it won&#39;t be me."

也許你們在想 「好吧，那不會是我。」

那麼，沒關係， 你會是那個照顧他的人。

this terrifying disease is likely to affect us all.

這個可怕的疾病 可能會影響我們每一個人。

Part of the fear around Alzheimer&#39;s stems from the sense

that there&#39;s nothing we can do about it.

部分源於我們對這疾病的無能為力。

Despite decades of research, we still have no disease-modifying treatment

儘管已有數十年的研究， 我們仍未找到改善它的治療方式，

So if we&#39;re lucky enough to live long enough,

Alzheimer&#39;s appears to be our brain&#39;s destiny.

罹患阿茲海默症似乎就是 我們大腦的宿命。

What if I told you we could change these statistics,

假如我說我們能改變這些數據，

literally change our brain&#39;s destiny,

without relying on a cure or advancements in medicine?

而不需要依靠任何 藥物的治療或改善呢？

Let&#39;s begin by looking at what we currently understand

about the neuroscience of Alzheimer&#39;s.

我們對阿茲海默症神經學上的了解。

Here&#39;s a picture of two neurons connecting.

The point of connection, this space circled in red,

它們的連結點， 也就是紅色圈的這個地方

The synapse is where neurotransmitters are released.

突觸就是神經傳導物釋放的地方。

This is where signals are transmitted, where communication happens.

訊號在這裡被傳遞、 產生交流的地方。

This is where we think, feel, see, hear, desire ...

這裡是我們思考、感覺、 看、聽、產生慾望......

And the synapse is where Alzheimer&#39;s happens.

而突觸也是阿茲海默症 發病的地方，

and look at a cartoon representation of what&#39;s going on.

During the business of communicating information,

in addition to releasing neurotransmitters like glutamate into the synapse,

除了釋放神經傳導物， 如：麩胺酸，到突觸中。

neurons also release a small peptide called amyloid beta.

神經元也會釋放一種小分子蛋白質， 叫作 β-類澱粉蛋白。

Normally, amyloid beta is cleared away metabolized by microglia,

通常，β-類澱粉蛋白 會被微膠細胞代謝清除，

微膠細胞就像我們大腦的清潔工。

While the molecular causes of Alzheimer&#39;s are still debated,

儘管分子層面引發 阿茲海默症的原因仍爭論不休，

most neuroscientists believe that the disease begins

但大多數的神經學家相信 此疾病發作的起源，

就是在 β-類澱粉蛋白 開始累積的時候。

Too much is released, or not enough is cleared away,

當他們被釋放太多， 或被清除掉的不夠多，

and the synapse begins to pile up with amyloid beta.

β-類澱粉蛋白就開始堆積在突觸。

And when this happens, it binds to itself,

forming sticky aggregates called amyloid plaques.

形成黏性凝聚物， 叫作澱粉樣蛋白斑。

How many people here are 40 years old or older?

現場有多少人的年紀 是 40 歲或以上？

this presence of amyloid plaques accumulating,

The only way we could be sure of this would be through a PET scan,

我們唯一可以確認的方法 是透過「正子掃描」，

because at this point, you are blissfully unaware.

You&#39;re not showing any impairments in memory, language, or cognition ...

你尚未有任何記憶、 語言或認知方面衰退的現象......

We think it takes at least 15 to 20 years of amyloid plaque accumulation

我們認為澱粉樣蛋白斑的累積 至少需要 15 到 20 年，

that causes the clinical symptoms of the disease.

而造成了阿茲海默症的臨床症狀。

your lapses in memory might include things like,

「我為甚麼要走進這個房間來？」

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 --

我知道你們中的半數， 在過去 24 小時之內

these are all normal kinds of forgetting.

至少曾經經歷過 上述的其中一件事情，

In fact, I would argue that these examples

because you didn&#39;t pay attention to where you put your keys

並不會去注意到 你把鑰匙放到哪裡。

the glitches in memory, language and cognition are different.

Instead of eventually finding your keys in your coat pocket

你的記憶、語言和認知上的偏差 就會變得不同了。

你最後才知道鑰匙 並非在你的外套口袋裡，

或者，你找到它後，你卻在想：

So what happens when amyloid plaques accumulate to this tipping point?

「這東西是用來做甚麼用的？」

Our microglia janitor cells become hyper-activated,

當澱粉樣蛋白斑累積到臨界點時， 到底會發生甚麼事？

releasing chemicals that cause inflammation and cellular damage.

我們的微膠細胞清潔工 會變得極度活躍，

We think they might actually start clearing away

它們會釋放出化學物質， 造成發炎和細胞的損壞。

A crucial neural transport protein called "tau" becomes hyperphosphorylated

and twists itself into something called "tangles,"

有一個重要的神經傳導蛋白叫做 「tau 蛋白」會被過磷酸化，

which choke off the neurons from the inside.

並把自己轉變成一種叫 「纖維纏結」的東西，

By mid-stage Alzheimer&#39;s, we have massive inflammation and tangles

我們的突觸會發生 大量的發炎並糾纏在一起，

So if you were a scientist trying to cure this disease,

at what point would you ideally want to intervene?

假如你是科學家， 試著要治療這個疾病，

Many scientists are betting big on the simplest solution:

最佳的介入時機是甚麼時候呢？

keep amyloid plaques from reaching that tipping point,

許多科學家賭在 最簡單的解決方案上：

which means that drug discovery is largely focused on developing a compound

避免澱粉樣蛋白斑累積到臨界點，

that will prevent, eliminate, or reduce amyloid plaque accumulation.

也就是說，大部分的 藥物治療主要是研究化合物

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【TED】Lisa Genova：預防阿爾茨海默症你能做什麼（預防阿爾茨海默症你能做什麼｜Lisa Genova）。 (【TED】Lisa Genova: What you can do to prevent Alzheimer's (What you can do to prevent Alzheimer's | Lisa Genova))