精选100篇经典TED演讲，时长8-15分钟，内容涵盖创新、成长与未来趋势。提供MP3在线播放、下载及英文文本，助你提升听力与口语。用思想的力量，点燃学习热情！下面是本期【TED】100篇经典演讲口语听力素材合集的内容，坚持积累，让你的英语更贴近生活！

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 use, and let's imagine that we're all 85. Now, everyone look at two people. One of you probably has Alzheimer's disease. Alright. And maybe you're thinking, well, it won't be me. Then, okay, you are a caregiver. So, in some way, this terrifying disease is likely to affect us all. Part of the fear around Alzheimer 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. 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, our 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, the 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 and 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.

How many people here are 40 years older 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. Now, 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. Yes. We think it takes at least 15 to 20 years of amyloid plaques 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? Yes. 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.

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 four? So what happens when amyloid plaques accumulate to this tipping point? Our microglia janitor cells become hyperactivated, 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.

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 seesaw 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. 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. 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 the ribose 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 your cell phone 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.

Cardiovascular health is another major factor. 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% 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 the scale.

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 neuroplasticity and cognitive reserve. Remember, the experience of having Alzheimer's is ultimately a result of losing synapses. The average brain has over 100 trillion synapses, which is fantastic. We've got a lot to work with. This isn't a static number. We gain and lose synapses all the time through a process called neuroplasticity. Every time we learn something new, we are creating and strengthening new neural connections, new 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 a mess. 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 emotions.