TED2017
Lisa Genova: What you can do to prevent Alzheimer's
麗莎．吉諾瓦: 你可以做些甚麼事，來預防老年癡呆症？
Filmed:
Readability: 4.8
4,830,426 views
神經科學家同時也是《我想念我自己》的作者麗莎．吉諾瓦 (Lisa Genova) 說，「老年癡呆症不一定是你大腦的宿命」。她向我們分享這個疾病最新的科學調查，以及一些前瞻性的研究，讓我們可以做些事來建構起一顆「對抗老年癡呆症的大腦」。
Lisa Genova - Neuroscientist, novelist
Through her fiction, Lisa Genova beckons us into the lives of people with neurological disease, making their worlds real and relatable. Full bio
Through her fiction, Lisa Genova beckons us into the lives of people with neurological disease, making their worlds real and relatable. Full bio
Double-click the English transcript below to play the video.
00:13
How many people here would like to live
to be at least 80 years old?
to be at least 80 years old?
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在場有多少人
希望能活到 80 歲以上？
希望能活到 80 歲以上？
00:18
Yeah.
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是的。
00:19
I think we all have
this hopeful expectation
this hopeful expectation
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我想我們都有這個期望，
00:22
of living into old age.
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期望能活得很久。
00:24
Let's project out into the future,
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讓我們穿越到未來，
00:26
to your future "you's,"
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想像一下未來的你們，
00:28
and let's imagine that we're all 85.
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想像我們現在全都已變成 85 歲。
00:31
Now, everyone look at two people.
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現在，每個人分別看向兩個人，
00:35
One of you probably has
Alzheimer's disease.
Alzheimer's disease.
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你們之中其中一個
可能就有阿茲海默症。
可能就有阿茲海默症。
00:39
(Laughter)
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（笑聲）
00:42
Alright, alright.
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好了，好了。
00:44
And maybe you're thinking,
"Well, it won't be me."
"Well, it won't be me."
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也許你們在想
「好吧，那不會是我。」
「好吧，那不會是我。」
00:49
Then, OK. You are a caregiver.
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那麼，沒關係，
你會是那個照顧他的人。
你會是那個照顧他的人。
00:53
So --
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所以......
00:54
(Laughter)
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（笑聲）
00:57
so in some way,
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所以就某方面而言，
00:58
this terrifying disease
is likely to affect us all.
is likely to affect us all.
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這個可怕的疾病
可能會影響我們每一個人。
可能會影響我們每一個人。
01:02
Part of the fear around Alzheimer's
stems from the sense
stems from the sense
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對於阿茲海默症的恐懼
部分源於我們對這疾病的無能為力。
01:05
that there's nothing we can do about it.
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01:08
Despite decades of research, we still
have no disease-modifying treatment
have no disease-modifying treatment
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儘管已有數十年的研究，
我們仍未找到改善它的治療方式，
我們仍未找到改善它的治療方式，
01:13
and no cure.
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也沒辦法徹底治癒它。
01:15
So if we're lucky enough
to live long enough,
to live long enough,
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所以假如我們有幸活得很久，
01:17
Alzheimer's appears to be
our brain's destiny.
our brain's destiny.
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罹患阿茲海默症似乎就是
我們大腦的宿命。
我們大腦的宿命。
01:21
But maybe it doesn't have to be.
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但也並非得如此。
01:23
What if I told you we could
change these statistics,
change these statistics,
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假如我說我們能改變這些數據，
01:26
literally change our brain's destiny,
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徹底改變我們大腦的宿命，
01:29
without relying on a cure
or advancements in medicine?
or advancements in medicine?
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而不需要依靠任何
藥物的治療或改善呢？
藥物的治療或改善呢？
01:33
Let's begin by looking at
what we currently understand
what we currently understand
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讓我們先看看目前
我們對阿茲海默症神經學上的了解。
01:36
about the neuroscience of Alzheimer's.
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01:39
Here's a picture
of two neurons connecting.
of two neurons connecting.
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這是兩個神經元連結的圖片。
01:42
The point of connection,
this space circled in red,
this space circled in red,
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它們的連結點，
也就是紅色圈的這個地方
也就是紅色圈的這個地方
01:46
is called the synapse.
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叫作突觸。
01:47
The synapse is where
neurotransmitters are released.
neurotransmitters are released.
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突觸就是神經傳導物釋放的地方。
01:51
This is where signals are transmitted,
where communication happens.
where communication happens.
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訊號在這裡被傳遞、
產生交流的地方。
產生交流的地方。
01:55
This is where we think,
feel, see, hear, desire ...
feel, see, hear, desire ...
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這裡是我們思考、感覺、
看、聽、產生慾望......
看、聽、產生慾望......
02:00
and remember.
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和記憶的地方。
02:02
And the synapse
is where Alzheimer's happens.
is where Alzheimer's happens.
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而突觸也是阿茲海默症
發病的地方，
發病的地方，
02:05
Let's zoom in on the synapse
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讓我們放大來看突觸，
02:07
and look at a cartoon representation
of what's going on.
of what's going on.
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看看這個現象的卡通示意圖。
02:10
During the business
of communicating information,
of communicating information,
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在傳訊的過程中，
02:13
in addition to releasing neurotransmitters
like glutamate into the synapse,
like glutamate into the synapse,
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除了釋放神經傳導物，
如：麩胺酸，到突觸中。
如：麩胺酸，到突觸中。
02:17
neurons also release a small peptide
called amyloid beta.
called amyloid beta.
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神經元也會釋放一種小分子蛋白質，
叫作 β-類澱粉蛋白。
叫作 β-類澱粉蛋白。
02:22
Normally, amyloid beta is cleared away
metabolized by microglia,
metabolized by microglia,
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通常，β-類澱粉蛋白
會被微膠細胞代謝清除，
會被微膠細胞代謝清除，
02:27
the janitor cells of our brains.
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微膠細胞就像我們大腦的清潔工。
02:30
While the molecular causes
of Alzheimer's are still debated,
of Alzheimer's are still debated,
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儘管分子層面引發
阿茲海默症的原因仍爭論不休，
阿茲海默症的原因仍爭論不休，
02:34
most neuroscientists believe
that the disease begins
that the disease begins
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但大多數的神經學家相信
此疾病發作的起源，
此疾病發作的起源，
02:37
when amyloid beta begins to accumulate.
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就是在 β-類澱粉蛋白
開始累積的時候。
開始累積的時候。
02:40
Too much is released,
or not enough is cleared away,
or not enough is cleared away,
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當他們被釋放太多，
或被清除掉的不夠多，
或被清除掉的不夠多，
02:43
and the synapse begins
to pile up with amyloid beta.
to pile up with amyloid beta.
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β-類澱粉蛋白就開始堆積在突觸。
02:47
And when this happens, it binds to itself,
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當此狀況發生，它就會凝結，
02:49
forming sticky aggregates
called amyloid plaques.
called amyloid plaques.
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形成黏性凝聚物，
叫作澱粉樣蛋白斑。
叫作澱粉樣蛋白斑。
02:53
How many people here
are 40 years old or older?
are 40 years old or older?
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現場有多少人的年紀
是 40 歲或以上？
是 40 歲或以上？
02:57
You're afraid to admit it now.
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現在大家都害怕承認了？
02:59
This initial step into the disease,
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這就是疾病的最初階段，
03:01
this presence of amyloid
plaques accumulating,
plaques accumulating,
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澱粉樣蛋白斑累積的現象
03:05
can already be found in your brains.
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可能已存在你們的大腦中，
03:08
The only way we could be sure of this
would be through a PET scan,
would be through a PET scan,
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我們唯一可以確認的方法
是透過「正子掃描」，
是透過「正子掃描」，
03:11
because at this point,
you are blissfully unaware.
you are blissfully unaware.
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因為現在你對此毫無知覺，
03:15
You're not showing any impairments
in memory, language, or cognition ...
in memory, language, or cognition ...
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你尚未有任何記憶、
語言或認知方面衰退的現象......
語言或認知方面衰退的現象......
03:19
yet.
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但……只是尚未。
03:21
We think it takes at least 15 to 20 years
of amyloid plaque accumulation
of amyloid plaque accumulation
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我們認為澱粉樣蛋白斑的累積
至少需要 15 到 20 年，
至少需要 15 到 20 年，
03:26
before it reaches a tipping point,
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才能到達臨界點，
03:28
then triggering a molecular cascade
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隨後引發分子的連鎖反應，
03:30
that causes the clinical
symptoms of the disease.
symptoms of the disease.
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而造成了阿茲海默症的臨床症狀。
03:33
Prior to the tipping point,
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在到達臨界點之前，
03:35
your lapses in memory
might include things like,
might include things like,
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你的記憶衰退可能會像這樣：
03:39
"Why did I come in this room?"
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「我為甚麼要走進這個房間來？」
03:41
or "Oh ... what's his name?"
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或「喔......他叫甚麼名字？」
03:44
or "Where did I put my keys?"
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或「我把鑰匙放在了哪裡？」
03:47
Now, before you all
start freaking out again,
start freaking out again,
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現在，在你們驚慌失措之前，
03:50
because I know half of you did at least
one of those in the last 24 hours --
one of those in the last 24 hours --
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我知道你們中的半數，
在過去 24 小時之內
在過去 24 小時之內
至少曾經經歷過
上述的其中一件事情，
上述的其中一件事情，
03:55
these are all normal kinds of forgetting.
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這些都是正常的遺忘症狀。
03:58
In fact, I would argue that these examples
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事實上，上述這些例子
04:01
might not even involve your memory,
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可能根本與你的記憶無關，
04:03
because you didn't pay attention
to where you put your keys
to where you put your keys
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因為你第一時間，
並不會去注意到
你把鑰匙放到哪裡。
你把鑰匙放到哪裡。
04:06
in the first place.
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04:07
After the tipping point,
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一旦臨界點發生之後，
04:09
the glitches in memory,
language and cognition are different.
language and cognition are different.
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你的記憶、語言和認知上的偏差
就會變得不同了。
就會變得不同了。
04:12
Instead of eventually finding
your keys in your coat pocket
your keys in your coat pocket
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你最後才知道鑰匙
並非在你的外套口袋裡，
並非在你的外套口袋裡，
04:15
or on the table by the door,
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也並非門旁的桌子上，
04:17
you find them in the refrigerator,
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而是你把它放在冰箱裡了，
04:20
or you find them and you think,
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或者，你找到它後，你卻在想：
04:22
"What are these for?"
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「這東西是用來做甚麼用的？」
04:24
So what happens when amyloid plaques
accumulate to this tipping point?
accumulate to this tipping point?
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當澱粉樣蛋白斑累積到臨界點時，
到底會發生甚麼事？
到底會發生甚麼事？
04:30
Our microglia janitor cells
become hyper-activated,
become hyper-activated,
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我們的微膠細胞清潔工
會變得極度活躍，
會變得極度活躍，
04:33
releasing chemicals that cause
inflammation and cellular damage.
inflammation and cellular damage.
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它們會釋放出化學物質，
造成發炎和細胞的損壞。
造成發炎和細胞的損壞。
04:37
We think they might actually
start clearing away
start clearing away
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我們認為它們正在清除的
04:40
the synapses themselves.
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就是突觸本身。
04:42
A crucial neural transport protein
called "tau" becomes hyperphosphorylated
called "tau" becomes hyperphosphorylated
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有一個重要的神經傳導蛋白叫做
「tau 蛋白」會被過磷酸化，
「tau 蛋白」會被過磷酸化，
04:46
and twists itself
into something called "tangles,"
into something called "tangles,"
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並把自己轉變成一種叫
「纖維纏結」的東西，
「纖維纏結」的東西，
04:49
which choke off the neurons
from the inside.
from the inside.
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從內部堵塞神經元。
04:52
By mid-stage Alzheimer's,
we have massive inflammation and tangles
we have massive inflammation and tangles
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到了中期的阿茲海默症，
我們的突觸會發生
大量的發炎並糾纏在一起，
大量的發炎並糾纏在一起，
04:56
and all-out war at the synapse
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04:58
and cell death.
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然後細胞就會死亡。
05:00
So if you were a scientist
trying to cure this disease,
trying to cure this disease,
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假如你是科學家，
試著要治療這個疾病，
試著要治療這個疾病，
05:03
at what point would you ideally
want to intervene?
want to intervene?
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最佳的介入時機是甚麼時候呢？
05:07
Many scientists are betting big
on the simplest solution:
on the simplest solution:
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許多科學家賭在
最簡單的解決方案上：
最簡單的解決方案上：
05:11
keep amyloid plaques
from reaching that tipping point,
from reaching that tipping point,
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避免澱粉樣蛋白斑累積到臨界點，
05:14
which means that drug discovery is largely
focused on developing a compound
focused on developing a compound
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也就是說，大部分的
藥物治療主要是研究化合物
藥物治療主要是研究化合物
05:18
that will prevent, eliminate, or reduce
amyloid plaque accumulation.
amyloid plaque accumulation.
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利用它們來預防、消除或減少
澱粉樣蛋白斑的累積。
澱粉樣蛋白斑的累積。
05:24
So the cure for Alzheimer's will likely be
a preventative medicine.
a preventative medicine.
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所以他們研發的藥物，
都只是一些預防老年癡呆的藥物。
都只是一些預防老年癡呆的藥物。
05:30
We're going to have to take this pill
before we reach that tipping point,
before we reach that tipping point,
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我們會在達到臨界點之前、
05:33
before the cascade is triggered,
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在分子連鎖反應產生之前、
05:35
before we start leaving
our keys in the refrigerator.
our keys in the refrigerator.
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在我們開始把鑰匙
遺忘在冰箱裡之前服用這些藥物。
遺忘在冰箱裡之前服用這些藥物。
05:39
We think this is why, to date,
these kinds of drugs have failed
these kinds of drugs have failed
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我們認為這是目前為止
這些藥物在臨床實驗中
這些藥物在臨床實驗中
05:43
in clinical trials --
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失敗的原因……
05:44
not because the science wasn't sound,
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並不是科學不夠可靠，
05:46
but because the people in these trials
were already symptomatic.
were already symptomatic.
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而是因為實驗對象都已經有症狀了。
05:50
It was too late.
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已經太遲了。
05:52
Think of amyloid plaques as a lit match.
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試想澱粉樣蛋白斑
是一根已經點燃的火柴棒。
是一根已經點燃的火柴棒。
05:55
At the tipping point, the match
sets fire to the forest.
sets fire to the forest.
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到了臨界點時，火柴棒點燃了森林。
05:59
Once the forest is ablaze,
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一旦森林著火，
06:01
it doesn't do any good
to blow out the match.
to blow out the match.
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把火柴棒吹熄已於事無補。
06:04
You have to blow out the match
before the forest catches fire.
before the forest catches fire.
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你必須在森林著火之前就吹熄火柴。
06:08
Even before scientists sort this out,
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即使科學家尚未找到解決方法，
06:10
this information is actually
really good news for us,
really good news for us,
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但這個消息確實振奮人心，
06:13
because it turns out that the way we live
can influence the accumulation
can influence the accumulation
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因為它證明了我們生活的方式
會影響澱粉樣蛋白的累積。
06:17
of amyloid plaques.
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06:18
And so there are things we can do
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我們可以做一些事情，
06:20
to keep us from reaching
that tipping point.
that tipping point.
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來避免自己達到臨界點。
06:23
Let's picture your risk
of Alzheimer's as a see-saw scale.
of Alzheimer's as a see-saw scale.
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讓我們把罹患老年癡呆的風險
比作是蹺蹺板。
比作是蹺蹺板。
06:27
We're going to pile
risk factors on one arm,
risk factors on one arm,
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我們把造成風險的因素
放在蹺蹺板的其中一邊，
放在蹺蹺板的其中一邊，
06:29
and when that arm hits the floor,
you are symptomatic
you are symptomatic
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當這一邊碰到地面，
那麼症狀就會出現，
那麼症狀就會出現，
06:31
and diagnosed with Alzheimer's.
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然後被診斷為阿茲海默症。
06:34
Let's imagine you're 50 years old.
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假設你已經 50 歲。
06:36
You're not a spring chicken anymore,
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你已不再年輕，
06:38
so you've accumulated
some amyloid plaques with age.
some amyloid plaques with age.
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隨著年紀增長，你已經
累積了一些澱粉狀蛋白班。
累積了一些澱粉狀蛋白班。
06:41
Your scale is tipped a little bit.
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你的蹺蹺板已稍微傾斜。
06:44
Now let's look at your DNA.
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現在我們來看看你的 DNA。
06:46
We've all inherited our genes
from our moms and our dads.
from our moms and our dads.
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我們從父母那裡繼承了基因。
06:50
Some of these genes will increase our risk
and some will decrease it.
and some will decrease it.
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有些基因會增加風險而有些會減少。
06:54
If you're like Alice in "Still Alice,"
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如果你們像電影《我想念我自己》
中的女主角愛莉絲一樣，
中的女主角愛莉絲一樣，
06:56
you've inherited a rare genetic mutation
that cranks out amyloid beta,
that cranks out amyloid beta,
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遺傳了罕見的基因突變，
不正常地大量增生 β-類澱粉蛋白，
不正常地大量增生 β-類澱粉蛋白，
07:01
and this alone will tip
your scale arm to the ground.
your scale arm to the ground.
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這會讓你的蹺蹺板一端墜落到地面，
07:04
But for most of us, the genes we inherit
will only tip the arm a bit.
will only tip the arm a bit.
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但對大多數人來說，
我們遺傳到的基因
只會讓蹺蹺板稍微傾斜。
只會讓蹺蹺板稍微傾斜。
07:08
For example, APOE4 is a gene variant
that increases amyloid,
that increases amyloid,
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舉例來說，APOE4 是一個
會增生澱粉樣蛋白斑的變種基因，
會增生澱粉樣蛋白斑的變種基因，
07:13
but you can inherit a copy of APOE4
from mom and dad
from mom and dad
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但你可能從父母那裡
遺傳了 APOE4，
遺傳了 APOE4，
07:16
and still never get Alzheimer's,
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卻不會得到阿茲海默症，
07:19
which means that for most of us,
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也就是說對大多數人來說，
07:21
our DNA alone does not determine
whether we get Alzheimer's.
whether we get Alzheimer's.
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光憑我們的 DNA 並不能決定
我們是否會得阿茲海默症。
我們是否會得阿茲海默症。
07:25
So what does?
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那麼甚麼能決定呢？
07:27
We can't do anything about getting older
or the genes we've inherited.
or the genes we've inherited.
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我們對於衰老無能為力，
也無法決定我們遺傳的基因。
也無法決定我們遺傳的基因。
07:31
So far, we haven't changed
our brain's destiny.
our brain's destiny.
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目前為止，我們仍無法改變
大腦的宿命。
大腦的宿命。
07:35
What about sleep?
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那麼睡覺呢？
07:37
In slow-wave deep sleep, our glial cells
rinse cerebral spinal fluid
rinse cerebral spinal fluid
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在慢波深眠中，我們的神經膠細胞
會在我們的大腦中，沖洗腦脊液。
07:41
throughout our brains,
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07:42
clearing away metabolic waste
that accumulated in our synapses
that accumulated in our synapses
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當我們清醒的時候，
07:46
while we were awake.
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它會清除掉累積在突觸的
代謝廢物。
代謝廢物。
07:48
Deep sleep is like
a power cleanse for the brain.
a power cleanse for the brain.
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深度睡眠就好像大腦的強效淨化。
07:51
But what happens if you shortchange
yourself on sleep?
yourself on sleep?
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假如你稍微改變
睡眠方式會發生甚麼事？
睡眠方式會發生甚麼事？
07:55
Many scientists believe
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許多科學家相信，
07:56
that poor sleep hygiene might actually
be a predictor of Alzheimer's.
be a predictor of Alzheimer's.
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糟糕的睡眠狀況
可能會導致阿茲海默症。
可能會導致阿茲海默症。
08:01
A single night of sleep deprivation
leads to an increase in amyloid beta.
leads to an increase in amyloid beta.
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僅僅一個晚上的睡眠不足就會導致
β-類澱粉蛋白的增生。
β-類澱粉蛋白的增生。
08:07
And amyloid accumulation
has been shown to disrupt sleep,
has been shown to disrupt sleep,
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而澱粉樣蛋白斑的累積
已被證實會干擾睡眠，
已被證實會干擾睡眠，
08:10
which in turn causes
more amyloid to accumulate.
more amyloid to accumulate.
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結果導致更多澱粉樣蛋白斑的累積。
08:13
And so now we have
this positive feedback loop
this positive feedback loop
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成為一個惡性循環，
08:15
that's going to accelerate
the tipping of that scale.
the tipping of that scale.
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加劇了蹺蹺板的傾斜。
08:19
What else?
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還有甚麼？
08:20
Cardiovascular health.
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心血管健康。
08:23
High blood pressure, diabetes,
obesity, smoking, high cholesterol,
obesity, smoking, high cholesterol,
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高血壓、糖尿病、過重、
抽菸、高膽固醇，
抽菸、高膽固醇，
08:26
have all been shown to increase our risk
of developing Alzheimer's.
of developing Alzheimer's.
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全都會增加罹患阿茲海默症的風險。
08:30
Some autopsy studies have shown
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病理剖析的研究報告顯示，
08:32
that as many as 80 percent
of people with Alzheimer's
of people with Alzheimer's
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罹患阿茲海默的人群中，
多達 80% 的病患，
多達 80% 的病患，
08:35
also had cardiovascular disease.
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同時擁有心血管疾病。
08:38
Aerobic exercise has been shown
in many studies to decrease amyloid beta
in many studies to decrease amyloid beta
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許多阿茲海默症的
動物模擬實驗研究中顯示，
動物模擬實驗研究中顯示，
08:43
in animal models of the disease.
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有氧運動可以減少
β-類澱粉蛋白的數量。
β-類澱粉蛋白的數量。
08:45
So a heart-healthy
Mediterranean lifestyle and diet
Mediterranean lifestyle and diet
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所以有益身心健康的
地中海式生活飲食方式，
地中海式生活飲食方式，
08:49
can help to counter
the tipping of this scale.
the tipping of this scale.
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可以幫忙抵抗蹺蹺板的傾斜。
08:52
So there are many things we can do
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所以我們有很多事可以做，
08:55
to prevent or delay
the onset of Alzheimer's.
the onset of Alzheimer's.
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來預防或延緩老年痴呆症的到來。
08:57
But let's say
you haven't done any of them.
you haven't done any of them.
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但假設你甚麼事都沒做。
09:00
Let's say you're 65;
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假設你已 65 歲；
09:02
there's Alzheimer's in your family,
so you've likely inherited a gene or two
so you've likely inherited a gene or two
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你有阿茲海默症的家族病史，
所以你很可能帶有阿茲海默基因，
所以你很可能帶有阿茲海默基因，
09:06
that tips your scale arm a bit;
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這會讓你的蹺蹺板傾斜一點點；
09:08
you've been burning the candle
at both ends for years;
at both ends for years;
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你已經蠟燭兩頭燒了好幾年；
09:11
you love bacon;
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你愛吃培根；
09:12
and you don't run unless
someone's chasing you.
someone's chasing you.
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你也不去跑步，除非有人在追你。
09:14
(Laughter)
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（笑）
09:16
Let's imagine that your amyloid plaques
have reached that tipping point.
have reached that tipping point.
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想像你的澱粉樣蛋白斑
已經累積到臨界點。
已經累積到臨界點。
09:19
Your scale arm has crashed to the floor.
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你的蹺蹺板已經墜落到地面。
09:21
You've tripped the cascade,
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你觸發了連鎖反應，
09:23
setting fire to the forest,
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引發了森林大火，
09:25
causing inflammation, tangles,
and cell death.
and cell death.
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你開始出現發炎、
神經纏結和細胞凋亡的情況。
神經纏結和細胞凋亡的情況。
09:29
You should be symptomatic for Alzheimer's.
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你的阿茲海默症已經病發。
09:31
You should be having trouble
finding words and keys
finding words and keys
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你開始會造詞困難、找不到鑰匙，
09:35
and remembering what I said
at the beginning of this talk.
at the beginning of this talk.
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記不得我在演講剛開始時
到底說了些甚麼。
到底說了些甚麼。
09:38
But you might not be.
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但你也可能不會這樣。
09:41
There's one more thing you can do
to protect yourself
to protect yourself
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你還可以做一件事來保護自己，
09:43
from experiencing
the symptoms of Alzheimer's,
the symptoms of Alzheimer's,
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來避免阿茲海默症狀出現，
09:46
even if you have the full-blown disease
pathology ablaze in your brain.
pathology ablaze in your brain.
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那怕你的大腦已病入膏肓，
09:50
It has to do with neural plasticity
and cognitive reserve.
and cognitive reserve.
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它仍然跟神經可塑性
和認知儲備有關。
和認知儲備有關。
09:55
Remember, the experience
of having Alzheimer's
of having Alzheimer's
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記住，老年痴呆症發作的根本原因
09:57
is ultimately a result of losing synapses.
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就是突觸已經被破壞了。
10:01
The average brain has
over a hundred trillion synapses,
over a hundred trillion synapses,
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大腦平均擁有超過百萬億個突觸，
10:04
which is fantastic;
we've got a lot to work with.
we've got a lot to work with.
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這很奇妙；我們要處理
這麼龐大的數目。
這麼龐大的數目。
10:07
And this isn't a static number.
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而這不是一個不變的數目。
10:09
We gain and lose synapses all the time,
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我們的突觸數目隨時都在增減，
10:11
through a process
called neural plasticity.
called neural plasticity.
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透過一個叫做
「神經可塑性」的過程。
「神經可塑性」的過程。
10:14
Every time we learn something new,
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每當我們學到新東西，
10:16
we are creating and strengthening
new neural connections,
new neural connections,
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我們就會創造和強化新的神經連結，
10:20
new synapses.
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和新的突觸。
10:22
In the Nun Study,
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在我們以修女為研究對象
進行的研究當中，
進行的研究當中，
10:24
678 nuns, all over the age of 75
when the study began,
when the study began,
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實驗開始時，678 位
全超過 75 歲的修女，
全超過 75 歲的修女，
10:29
were followed for more than two decades.
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將會被追蹤調查超過 20 年。
10:31
They were regularly given
physical checkups and cognitive tests,
physical checkups and cognitive tests,
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她們會定期接受
健康檢查和認知測試，
健康檢查和認知測試，
10:35
and when they died, their brains
were all donated for autopsy.
were all donated for autopsy.
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當她們死後，她們的大腦
會捐贈出來做病理解剖。
會捐贈出來做病理解剖。
10:39
In some of these brains, scientists
discovered something surprising.
discovered something surprising.
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科學家們在其中一些大腦中
發現了不可思議的東西。
發現了不可思議的東西。
10:43
Despite the presence of plaques
and tangles and brain shrinkage --
and tangles and brain shrinkage --
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儘管那些大腦中有澱粉樣蛋白斑、
神經纏結和大腦收縮的情況，
神經纏結和大腦收縮的情況，
10:48
what appeared to be
unquestionable Alzheimer's --
unquestionable Alzheimer's --
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這很明顯的，根本就是
阿茲海默症的典型病狀，
阿茲海默症的典型病狀，
10:51
the nuns who had belonged
to these brains showed no signs
to these brains showed no signs
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但擁有這些大腦的修女，
她們在世時，
她們在世時，
卻沒有表現出阿茲海默症的症狀。
10:54
of having the disease
while they were alive.
while they were alive.
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10:58
How can this be?
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怎麼會這樣？
11:00
We think it's because these nuns
had a high level of cognitive reserve,
had a high level of cognitive reserve,
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我們認為那是因為這些修女
擁有高度的認知儲備量，
擁有高度的認知儲備量，
11:04
which is a way of saying that they had
more functional synapses.
more functional synapses.
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也就是說他們有較多
運作良好的突觸。
運作良好的突觸。
11:08
People who have more years
of formal education,
of formal education,
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接受正規教育較多年的人、
11:10
who have a high degree of literacy,
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擁有較高學歷的人、
11:12
who engage regularly
in mentally stimulating activities,
in mentally stimulating activities,
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和會定期參與
促進精神刺激活動的人，
促進精神刺激活動的人，
11:16
all have more cognitive reserve.
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都會有較多的認知儲備量。
11:19
They have an abundance
and a redundancy in neural connections.
and a redundancy in neural connections.
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他們有充裕的神經連結。
11:23
So even if they have a disease
like Alzheimer's
like Alzheimer's
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所以即使他們因為患有像
阿茲海默那樣的疾病，
阿茲海默那樣的疾病，
11:25
compromising some of their synapses,
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使她們減少了一些突觸，
11:28
they've got many extra backup connections,
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她們還有很多備用的連結，
11:31
and this buffers them from noticing
that anything is amiss.
that anything is amiss.
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從而減緩她們的大腦產生混亂。
11:34
Let's imagine a simplified example.
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讓我們假想一個簡單的例子。
11:37
Let's say you only know one thing
about a subject.
about a subject.
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假設你對一個主題只有一個認知。
11:40
Let's say it's about me.
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假設那個主題就是我。
11:41
You know that Lisa Genova
wrote "Still Alice,"
wrote "Still Alice,"
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你知道麗莎．吉諾瓦寫了一本
《我想念我自己》，
《我想念我自己》，
11:43
and that's the only thing
you know about me.
you know about me.
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而這是你對我唯一的認知。
11:46
You have that single neural connection,
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你對我的認知，
只有單一個神經連結，
只有單一個神經連結，
11:48
that one synapse.
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單一個突觸。
11:50
Now imagine you have Alzheimer's.
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現在假設你有阿茲海默症。
11:52
You have plaques and tangles
and inflammation
and inflammation
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你有澱粉樣蛋白斑、
神經纏結和發炎的情況，
神經纏結和發炎的情況，
11:55
and microglia devouring that synapse.
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你的微膠細胞吞噬了突觸。
11:58
Now when someone asks you,
"Hey, who wrote 'Still Alice?'"
"Hey, who wrote 'Still Alice?'"
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現在當有人問你，
「嘿，誰寫了《我想念我自己》？」
「嘿，誰寫了《我想念我自己》？」
12:02
you can't remember,
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你不記得了，
12:04
because that synapse
is either failing or gone.
is either failing or gone.
235
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因為那個突觸不是失效就是不見了，
12:07
You've forgotten me forever.
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你就會永遠忘記我。
12:09
But what if you had learned more about me?
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但假如你對我了解更深呢？
12:12
Let's say you learned
four things about me.
four things about me.
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比如，你了解我四件事情。
12:14
Now imagine you have Alzheimer's,
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現在想像一下，你得了阿茲海默症，
12:16
and three of those synapses
are damaged or destroyed.
are damaged or destroyed.
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其中三個突觸被破壞了。
12:20
You still have a way
to detour the wreckage.
to detour the wreckage.
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你仍有一條可以繞過那些
被破壞的突觸的路線。
被破壞的突觸的路線。
12:22
You can still remember my name.
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你仍能記得我的名字。
12:25
So we can be resilient
to the presence of Alzheimer's pathology
to the presence of Alzheimer's pathology
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所以當我們有阿茲海默症的
病理狀況發生，
病理狀況發生，
12:29
through the recruitment
of yet-undamaged pathways.
of yet-undamaged pathways.
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藉由使用那些尚未受損的神經通道，
我們仍有可能可以復原，
我們仍有可能可以復原，
12:32
And we create these pathways,
this cognitive reserve,
this cognitive reserve,
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我們可以藉由學習新事物，
12:36
by learning new things.
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創造出新的通路、
增加認知的儲備量。
增加認知的儲備量。
12:38
Ideally, we want these new things
to be as rich in meaning as possible,
to be as rich in meaning as possible,
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理想上，我們希望這些新事物
越有豐富的意義越好，
越有豐富的意義越好，
12:43
recruiting sight and sound
and associations and emotion.
and associations and emotion.
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越能喚起我們的視覺、
聽覺、聯系和情感越好。
聽覺、聯系和情感越好。
12:48
So this really doesn't mean
doing crossword puzzles.
doing crossword puzzles.
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我的意思並非要你去做拼字遊戲。
12:51
You don't want to simply retrieve
information you've already learned,
information you've already learned,
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你不會想只是重拾你
已學習過的記憶，
已學習過的記憶，
12:55
because this is like traveling
down old, familiar streets,
down old, familiar streets,
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因為這就好比遊覽
老舊而熟悉的街頭，
老舊而熟悉的街頭，
12:59
cruising neighborhoods you already know.
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那些周邊環境你已了然於心。
13:02
You want to pave new neural roads.
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你要鋪設新的神經通路。
13:04
Building an Alzheimer's-resistant brain
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建造一個能抵禦阿茲海默症的大腦，
13:07
means learning to speak Italian,
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像是去學習義大利語、
13:09
meeting new friends,
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去交新朋友、
13:11
reading a book,
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讀一本書，
13:12
or listening to a great TED Talk.
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或聆聽超讚的 TED 演講。
13:15
And if, despite all of this, you are
someday diagnosed with Alzheimer's,
someday diagnosed with Alzheimer's,
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假如，儘管做了這些事，
你還是會在某一天
被診斷出阿茲海默症，
被診斷出阿茲海默症，
13:20
there are three lessons I've learned
from my grandmother
from my grandmother
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我從我祖母
和許多我認識的阿茲海默症患者
那兒學到了三件事。
那兒學到了三件事。
13:23
and the dozens of people I've come to know
living with this disease.
living with this disease.
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13:28
Diagnosis doesn't mean
you're dying tomorrow.
you're dying tomorrow.
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被診斷出阿茲海默症
並不代表你明天就會死掉。
並不代表你明天就會死掉。
13:31
Keep living.
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繼續活下去。
13:33
You won't lose your emotional memory.
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你不會喪失你的情感記憶。
13:35
You'll still be able
to understand love and joy.
to understand love and joy.
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你仍能理解愛與歡樂。
13:38
You might not remember
what I said five minutes ago,
what I said five minutes ago,
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你可能不會記得
五分鐘前我說了甚麼，
五分鐘前我說了甚麼，
13:42
but you'll remember how I made you feel.
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但你會記得我讓你感受到了甚麼。
13:44
And you are more than what
you can remember.
you can remember.
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你本身，比你能記得的
東西更有意義。
東西更有意義。
13:48
Thank you.
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謝謝。
13:49
(Applause)
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（掌聲）
ABOUT THE SPEAKER
Lisa Genova - Neuroscientist, novelistThrough her fiction, Lisa Genova beckons us into the lives of people with neurological disease, making their worlds real and relatable.
Why you should listen
Lisa Genova wields her ability to tell a story and her knowledge of the human brain to talk about medical conditions like Alzheimer’s in warmly human terms. Her writing, often focusing on those who are misunderstood, explores the lives of people living with neurological diseases and disorders. A bestselling author, her work has been transformed into an Oscar-winning film, Still Alice, but the real triumph is Genova’s ability to help us empathize with a person’s journey we otherwise couldn’t even begin to understand.
Her newest book, Inside the O’Briens, is about Huntington’s disease.
Lisa Genova | Speaker | TED.com