评论
打印
Scientists might be completely wrong about Alzheimer's.
关于阿尔茨海默症，科学家们可能都想错了。
It's among the leading causes of death in the U.S., but despite decades of study,
阿尔茨海默症是美国致命疾病之一，但经过几十年的研究
doctors still don't know how to slow the progression of neurodegeneration and dementia, let alone stop it.
医生们还是不知道如何减缓神经衰退和痴呆的进程，更别提阻止这种疾病了。
And that might be because, according to a massive study published yesterday in the journal Neuron,
这或许是因为，根据昨天发表在《Neuron》上的一项大规模研究发现，
the prevailing hypothesis of how the disease starts is wrong.
关于这种疾病如何开始的主流假设是错的。
Maybe it's not all about protein buildup. Maybe there are viruses, too.
或许这并不全是因为蛋白质的形成，或许也有病毒的参与。
And if the findings hold up against further scrutiny, that could change everything.
如果这些发现能够经得住未来各种审查的考验，那么一切都会被改变。
The most popular idea for how Alzheimer's starts is the amyloid cascade hypothesis.
关于阿尔茨海默症最主流的想法是淀粉样肽级联假说。
It says the disease stems from the overproduction or accumulation of proteins called beta-amyloid,
这种假说表示这种疾病源于一种叫做β-淀粉样蛋白的过度生产或积累，
which clump together into plaques in the brain.
生产出的β-淀粉样蛋白聚在一起在大脑中形成斑块。
These plaques lead to the formation of tangles of fibrous tau proteins, and ultimately cause the death of neurons.
这些斑块导致纤维T蛋白的混乱，最终导致神经元死亡。
The trouble is, pharmaceutical companies have been cooking up drugs that reduce amyloid-beta production or clear out plaques for years,
问题是制药公司一直在制造药物谎称能够减少淀粉样蛋白的产生或是清除斑块，
and none of them have stopped or slowed the disease in people.
但是这些药物并不能阻止或减缓人体的疾病。
So the researchers behind yesterday's study decided to come at the problem from a different angle.
因此参与那项研究的研究人员决定从不同角度研究这个问题。
Instead of starting with amyloids or any other idea about how the disease starts or progresses, they used mathematical models.
他们没有从淀粉样蛋白或任何其他关于疾病开始或进程的角度开始，而是使用了数学模型。
The upside of this approach is that it doesn't require assumptions about what's happening.
这种方法的优势是它不需要对意外事件进行任何假设。
Instead, it relies on massive amounts of data about everything,
相反，它依赖于有关一切事物的大规模数据，
from the genes and their expression levels all the way down to visible symptoms of the disease, to explain what's going on.
从基因和基因表达水平到疾病的明显症状，以解释其中原理。
This method takes a lot of data, and they were able to get it through brain banks —
这种方法需要大量数据，能够通过大脑银行，即
collections of brain tissue samples from people who elected to donate their brains for research after they died.
决定在死后将大脑捐献研究的那些捐赠者，他们大脑的脑组织样本收集。
Because they wanted to spot things that initiate Alzheimer's,
因为他们想窥探那些触发老人痴呆症的病因，
the scientists compared healthy brain tissue to those from people who had plaques and tangles in their brains but didn't have symptoms yet.
所以科学家们将健康大脑组织和那些大脑中有斑块但还未发病的人的脑组织进行对比。
So they had the disease, but it was early on—that way, the team wouldn't be misled by things that happen in the brain later as a result of the disease.
所以这些人有这种疾病，只是还没有发病，团队就不会被疾病所导致的病症所误导。
And they specifically looked for networks of genes that were behaving very differently in these early Alzheimer's brains and healthy controls,
他们明确地在这些早期老人痴呆症大脑和健康控制中表现异常的基因网路
and for the genes that were driving those differences.
以及那些驱动差异产生的基因。
Turns out, many of these genes were also ones that get dialed up or down when you're infected with a virus.
事实证明，很多这些基因也是那些受病毒感染影响的基因。
So, much to their surprise, their data-driven approach implicated viruses.
所以让他们惊讶的是，他们的数据驱动方法暗指病毒参与其中。
And while that might seem out of left field, the idea that microbes might be behind Alzheimer's isn't new — in fact, it's been around for at least half a century.
虽然这似乎有些出乎意料，关于细菌或许导致老人痴呆症的想法并不新鲜—事实上，这种想法存在至少半个世纪。
Some scientists have noticed links between various infections and Alzheimer's disease,
一些科学家注意到各种感染和老性痴呆之间的联系，
like that some infections can cause plaques to form in animal models, or that certain microbes show up more often in diseased brains.
比如，一些感染会引起斑块形成动物模型，或者在受疾病所困扰的大脑中，某些细菌出现更加频繁。
These links were compelling enough for them to propose an alternate model for Alzheimer's: the pathogen hypothesis,
这些联系令人信服，所以能够为老人痴呆症提出一种选择模型：病原体假设，
which says the plaques are just part of the disease — not the cause.
这种假设表示斑块只是这种疾病的一部分—而非病因。
But the idea hasn't gotten much traction in the field.
但是这种想法在这个领域并未得到多少牵引。
So as soon as the team from this new study saw a connection to viruses, they knew they had to dig a little deeper.
所以只要这支团队从这项新研究中观察到和病毒的一丝联系，就知道他们需要再往深处探究。
They checked for evidence of more than 500 viruses in four different brain regions in over 600 brain samples.
他们在六百多个大脑样本中的四块不同区域检查五百多种病毒的证据。
The results showed that two viruses in particular, which were types of human herpes viruses, were elevated in Alzheimer's brains.
结果显示有两种人类疱疹病毒从老人痴呆症大脑中显现。
Despite the name, these aren't the viruses behind genital herpes, and instead are most closely related to the strain behind roseola,
虽然名字如此，但是这些并不是生殖器疱疹，相反它们和蔷薇疹比较相关，
a rash and fever common in young children.
蔷薇疹常见于儿童的一种皮疹和发烧。
They screened brains from other brain banks, too—
他们又从其他大脑银行中扫描大脑
more than 900 brains all together—and those Alzheimer brains also had lots of these viruses.
一共扫描了九百多种—那些老人痴呆症大脑也有很多这种病毒。
But they weren't done. By itself, the data they'd gathered was just another correlation. It might not mean anything.
但是他们搜集的这些数据只不过是另一种关联。这或许说明不了什么。
So they did a bunch of tests to see if the evidence, as a whole, was consistent with the idea that these viruses could play a role in Alzheimer's—and it was.
所以他们做了很多测试检测这些证据是否与这样一种想法相关联—这些病毒也应对老人痴呆症负责—确实如此。
The more genetic material people had in their brains from these viruses, the more severe the disease was.
人们的大脑中这种病毒基因材料越多，病情越严重。
The team also found that certain small differences in people's DNA might be allowing the viruses to do more damage.
团队还发现某种人体DNA小差异或许跟着病毒对人体造成更多损害。
In other words, in their view, those at highest risk for Alzheimer's are likely to be people who have certain genetic predispositions combined with a viral infection.
换句话说，他们认为那些患老人痴呆症风险最高的人群可能就是那些某种遗传素质和某种病毒感染所相关的人。
They even tried an experiment on mice where they removed one of the genes turned down by one of these viruses, and that led to an increase in brain plaques.
他们甚至用老鼠做实验，他们移除了被这些病毒排除的基因之一，这些基因也会导致大脑斑块的增加。
So, the team did a lot of investigating, and the results strongly suggest that viruses are at least partially to blame for the disease.
因此团队做了很多调查，并且这些结果强烈暗示病毒至少对这种疾病负部分责任。
But it's important to note that this isn't proof of causation.
但是需要注意的是这并不能作为因果关系的证据。
The researchers were very clear about that. So it's way too early to declare war on herpes viruses to fight Alzheimer's.
研究人员对这一点非常清楚。但是要对疱疹病毒宣战对抗老人痴呆症还过早。
For example, this might be a weird side effect that happens because Alzheimer's somehow makes people more susceptible to brain infections really early on.
例如，这或许是一个怪异的副作用，因为老人痴呆症更易受大脑感染的影响。
Or, it's possible that the viruses are involved somehow in making symptoms worse, but aren't the actual trigger of the disease.
或许病毒让这些症状更加严重，但是却并不是触发这种疾病的真正原因。
Basically, there are a lot of hints that viruses might be to blame in some capacity, but it's not clear how this translates clinically.
基本上有多都暗示病毒或许在某种程度上应为疾病负责，但是还不清楚临床上如何转化。
No matter what, the full picture is going to be complicated.
不论怎样，整体过程很复杂。
It's entirely possible that what we call Alzheimer's is triggered or progresses in multiple ways — so the viruses could be involved in some cases but not others.
我们说老人痴呆症的病因或过程有很多种—所以病毒可能参与其中某些情况，但也不排除其他情况，这也是完全有可能的。
And maybe the person's immune system matters, too.
或许人类的免疫系统也有关。
Either way, this new study means scientists have a lot to think about.
不管怎样，这项新研究意味着科学家们有很多需要思考的。
And since the researchers stumbled upon the viral link using an unbiased method,
由于科学家们是利用无偏估方法偶然发现病毒的关联，
it may win over enough skeptics to get funding for more experiments, like a clinical trial.
这或许说服了很多怀疑论者筹集更多试验基金，比如临床实验。
And that just might lead to a whole new way of thinking about Alzheimer's—and eventually, ways to prevent or treat it.
这或许指向一个全新的思考老人痴呆症的新方法，最终能够预防或治愈这种疾病。
Thanks for watching this episode of SciShow!
感谢收看《科学秀》！
And an extra special thanks to our perennial President of Space, SR Foxley, for supporting us on Patreon. We really appreciate that.
特别感谢Space总裁 SR Foxley，感谢对我们的支持。非常感谢。
If you want to understand the science behind the latest headlines, or just get to know this universe a little better, stick around!
如果你想了解更多近期科学头条或这个宇宙，来吧！
We publish a new episode every single day, so go to youtube.com/scishow to subscribe.
我们每天都发布新视频，登录youtube.com/scishow订阅。
