Today, Explained - Good news about Alzheimer’s

Episode Date: September 16, 2026

Alzheimer’s research has stalled for decades. That’s finally changing. This episode was produced by Miles Bryan, edited by Amina Al-Sadi, fact-checked by Hady Mawajdeh and Avishay Artsy, engineered by Bridger Dunnagan and David Tatasciore, and hosted by Sean Rameswaram. This episode was produced in partnership with Vox's Future Perfect. A scan of the brain of a patient affected by Alzheimer's disease. Photo by BSIP/UIG via Getty Images. Listen to Today, Explained ad-free by becoming a Vox Member: vox.com/members. New Vox members get $20 off their membership right now. Transcript at ⁠⁠vox.com/today-explained-podcast⁠.⁠ Learn more about your ad choices. Visit podcastchoices.com/adchoices

Alzheimer's disease is uniquely terrifying to many people, in part because it gradually causes people to lose their sense of who they are. It's a gradual process, losing your keys, or having a hard time remembering the name of an old friend or someone who you knew a long time ago, to increasingly losing everyday memories that allow you to navigate the world, including where you are in your, town, even in your home when it gets worse. And when you start to lose those memories, you also start to lose your relationships with people. It becomes a disease that is very cruel in the way it captures your sense of self. Good news for people who hate Alzheimer's coming up on today, Explain from Vox. Volvo is leaving the chaos of rush hour outside.

Start by settling into your saddle-stitched Napa leather seats. Notice the open space around you. Uncluttered, elegant, intentional, warm ambient light, and natural wood details to ground you. This is Volvo's Scandinavian sanctuary for every journey. Learn more at volvocars.cares.cai, optional features mentioned. I'm Ina Garden. I have a new podcast called Happy Hour with Aina. Each week I'm inviting a really interesting guest to join me for a drink and a fun

conversation at my kitchen table in New York City. I'll be getting personal with actors, chefs, comedians, musicians, and writers I admire. So grab a snack, pull up a chair, and join us. You can watch by searching for a happy hour with Ina on YouTube or listen wherever you get your podcast. Don't we all need to have more fun? Today explained Sean Ramos from something like 7 million Americans have Alzheimer's, something like 50 million people around the world. And those aren't quite cancer numbers, but think of how many treatments we have for cancer. Surgery, chemo, radiation, immunotherapy, stem cell transplants. The list goes on. But Alzheimer's, the list is short. A couple of treatments to slow it down, nothing to roll it back, and certainly nothing close to a cure

for the disease thus far. We asked Science Magazine investigative journalist Charles Pillar, why that is. So in order to understand the answer to that, let me take you back actually more than 100 years. To the when Alzheimer's was named its namesake scientist, LOS Alzheimer, he did an autopsy of a woman who had terrible dementia. And what he found in her brain were two kinds of proteins. One he called plaques and one tangles. Placks are. something called amyloid protein, and tangles are made up of this protein called tau. So the disease was defined as plaques, tangles, and dementia. That's Alzheimer's disease. Now, at the time, in the early 1900s, it was more of a curiosity than anything else, because not that many people reached the very old age

where Alzheimer's would normally kick in. And so what you had was a very small number of people who reached that old age and got Alzheimer's disease. So people were interested, neurologists were interested in it way back then. But it wasn't a big, huge medical problem the way it is today. But then, over the decades, you have the development of vaccines and antibiotics and treatments for a lot of other important diseases like heart disease, cancer, and diabetes. And suddenly, you had this explosion of people living into their 60s, 70s, 80s, into the period of life, when Alzheimer's becomes common. So this doesn't become that big a problem until life starts getting better and longer for people.

That's right. That's right. It's a problem that's existed for hundreds, thousands of years, but in very small numbers. Back in the 70s, 80s, 90s, there was a lot of effort to try to look at what the underlying causes of Alzheimer's disease were. And that's when the development of something called the amyloid cascade hypothesis came onto the scene. Next tonight, a new development in understanding and possibly treating Alzheimer's disease. In this study, what the focus was on, a particular protein, beta amyloid, which when injected into the brains of laboratory animals, was found to induce very similar types of abnormal changes as is seen in Alzheimer's disease, specifically nerve cell damage and degeneration. And so the idea behind this theory, which is a beautiful theory of the disease,

is that the development, the deposits of amyloid proteins that cause these plaques in the brain, lead to a series of biochemical events in the brain that eventually cause Alzheimer's dementia. When this started happening, people were looking for the logical way of approaching it. And that was, let's get rid of the plaques. Let's get rid of these plaques that we believe are the linchpin of the disease, the thing that kicks off this cascade of events. And so in the 90s and the early 2000s, there was an enormous amount of effort put into the idea of creating drugs and even a vaccine that strip these plaques out of the brain. Trials of a vaccine against the brain disorder Alzheimer's disease have produced highly encouraging results. BBC News, July 2000.

And they found that they could pretty efficiently remove these plaques from the brain. But unfortunately, they found also that they were not able to get the benefits they thought they were going to get from this. A once promising vaccine failed to prevent the progression of Alzheimer's, even though it cleared dementia-linked amyloid plaques in the brain. ABC News, July 2008. People were just suffering the way they had been. And so there was a lot of discouragement by the early 2000s. There was a lot of discouragement. Maybe we're not on the right path.

Now, if you'd like, this is where I could bring in a description of my investigative findings and how they relate to the development of the field at this point. Would that be a good idea? Please, do tell. Okay, okay. Let's go for it. This is in the early 2000s, and what we're seeing is the, the success in removing plaques from the brain. But not only were people not getting better,

their symptoms weren't being improved or reversed, but people were also experiencing terrible side effects from some of these drugs. In fact, they were very dangerous at times. And consequently, the field was not just confused. They were troubled that maybe we're on the wrong path. Maybe we need to rethink things. And that's when a kind of brilliant experience, was done at the University of Minnesota, where they extracted a certain type of amyloid protein from the brain of mice. And then they used this particular protein called amyloid beta star 56, their star protein. And they injected into rats. And what they found was that these rats exhibited memory loss symptoms that were described as being similar to the memory loss we see with Alzheimer's

patients. And so what you had was for the first time, a very specific type of amyloid protein. And it seemed to be exhibiting a cause and effect relationship to memory loss. So the field was pretty excited about this because they thought, well, maybe we've been on the right path all along, but we've been looking at the wrong type of amyloid protein. We would have been attacking things maybe in the wrong way. We need to develop drugs that would have a more direct effect on this certain type of protein. which is called oligomer proteins.

These are soluble amylate proteins that float around in the cerebrospinal fluid that baths the brain. So they thought, well, you know, we can attack those. We can attack the plaques. Maybe we need to develop better drugs that would do that. And so a new resurgence of effort was put into developing these drugs that would have those potentially beneficial effects. This went on for years. And billions of dollars was put into it, not just into, research, but into drug developments. So you have to remember that drug companies spend enormous

sums of money to develop and test remedies that would then be suitable for approval by the Food and Drug Administration. When I entered the picture was back in 2022, and I was working, doing investigative research for a story on Alzheimer's disease. And I crossed paths with a scientist who was looking at Alzheimer's research and looking at the images that are produced within that research. And so what's really important to remember here is that this scientist, his name is Matthew Shrague at Vanderbilt University, he encountered this seminal report, this seminal study that appeared in nature, a journal that is one of the most eminent and important scientific journals. And what he looked at is the scientific images that were described in this experiment where they found this particular type of amyloid protein injected into rats, saw that the rats had memory problems.

And they found that the scientific images within this paper, and you have to remember that these images are in effect the data of the experiment. The scientific images were based on apparent image doctoring. In other words, they were changed in a way. to support the experimental hypothesis but was not actually demonstrated in the real data that was produced by the experiment. And a global developing story of what could be the biggest medical scandal in decades. The allegations in Science magazine

are reverberating through the science community and beyond. So this is to say that this amyloid beta star 56 wasn't as important as people thought. This was to say that the experiment that purported to show the great advance of amyloid beta star 56 was based on apparently doctored images. And eventually, the doctoring was proven and the paper was retracted. And so what I learned in this process is that the basis for the amyloid hypothesis, one of the seminal studies, I should say, was based on false information.

How much time and money has been spent? chasing this hypothesis? Let's just say that tens of billion of dollars have been put into the field. Probably the majority of that overall into amyloid-related product development and

basic research. And because we haven't seen any benefits that are really on the par of things that are curative for the disease, on the part of things that would at least stop the disease in its tracks, I think we have cause to wonder if that money was well spent, partly because there are other ideas

about Alzheimer's disease that have gotten short shrift as a result of the emphasis on this one way of looking at it. That was Charles Pillar. He wrote a book about all this called doctored, fraud, arrogance, and tragedy in the quest to cure Alzheimer's. And I know we promised you good news and so far all we've delivered is bad, but you had to understand the bad to appreciate the good that's coming next on today's explained. Support the showery comes from Chyne. Is your summer fun catching up with you? A weekend trip here,

a dinner there, spritzes on the patio that each cost double digits, you lush? Don't get me wrong, it was all worth it, but you might be feeling the financial squeeze going into fall, And that is where Chime comes in. Chime wants to change the way people bank. They're not like your old traditional banks, your dad's bank who charges fees and gate keeps perks and rewards. Chime, on the other hand, offers the most rewarding fee-free banking, all with no overdraft fees, no monthly fees, no minimum balance fees. You can join the millions who are already banking fee-free with American. is the number one choice for banking. Add to chime.com slash explained. That is chime.com

slash explained. You can sign up now for chime. It only takes a few minutes. Chime is a fintech, not a bank, banking services and chime card provided by Chim's bank partners. Qualifying direct deposits required. Terms and limits apply. Go to chime.com slash disclosures for details. Today explained is back. Charles has gone, but Dylan Scott from Vox is here. And Dylan, We have promised our audience good news. So far, they've only kind of heard bad news. So hit them with the good. Well, look, things have changed a lot in the last couple of years.

And there's a couple of reasons for that. We've actually got two treatments that if somebody walks into a clinic right now and is diagnosed with Alzheimer's disease, that doctors can offer them that will hopefully have some effect in slowing down their cognitive decline. And that's huge, because for a long time, we had nothing to offer people who had Alzheimer's disease. The drug development pipeline is also starting to look much more robust.

And then because of both of those things, you know, as one of the doctors I talked to in the last couple of weeks put it to me, like when you have a treatment, you have to be able to test for the disease that the treatment is supposed to address. And so there's been a lot of investment in manpower, in money into detecting Alzheimer's disease. coming up with blood tests that can tell you, even though sitting here today, you might not be exhibiting any symptoms that you are at a higher risk of developing Alzheimer's disease. Maybe that allows you to make lifestyle changes. Maybe that allows you to get on a medication earlier.

But the point is from having treatments that we can actually offer people and hopefully even better treatments in the pipeline and these early detection tools that are going to allow people to get ahead of this disease earlier and hopefully improve their outlook. You know, one of the doctors I talked to said it's been revolutionary. Okay. We love to hear some good news. You mentioned two treatments. Tell us what they are, Dylan?

So we have two drugs right now that have been approved by the FDA. There is lacanamab and dinanamab. We are our memories, so I want to hold on to them as long as I can. An anti-amiloid treatment for early symptomatic Alzheimer's disease, proven to slow the progression of the disease. And these are drugs that target the... amyloid plaque in the brain that scientists have a long thought might be associated with the development of Alzheimer's disease. Yes, our buddy Charles told us all about them, but he also told us about this fraudulent research around them. Are we good with this? The amyloid hypothesis has been

very controversial for a while, in part because there were these years and years where we weren't seeing any progress, despite this being the dominant hypothesis about the disease. But we do have these two drugs that in clinical trials have been shown to both clear out the amyloid plaque in somebody's brain, and they do seem to lead to slower cognitive decline for those patients. Okay. And the hope is that, like, this is the ground floor. This is the, these are the worst drugs, hopefully, that we're ever going to have. And continued, you know, scientific discovery and progress with developing drugs will lead to

even better treatments in the future. So tell us more about the scientific discovery. because you mentioned that there's promising research beyond, I'm guessing, these amyloid plaques? Yeah, I would say that it's not like the amyloid hypothesis has been invalidated. But I think our understanding of the disease, what's happened is it's become more complex. And we're realizing that there's probably also a role for a different kind of protein called tau. There may also be a role with chronic inflammation, your vascular health, your body's ability to just pump blood, blood, through your body may also be playing a role in the development of Alzheimer's disease.

And so now we're starting to see treatments that target these other things. In particular, it's like, the way I've been thinking about it is if we used to be putting all of our bets on amyloid, we're still putting some bets on amyloid, but we're also putting bets on these other things. And so now there are treatments in the works targeting, for example, these tau proteins. And they're still in like the early stages of clinical trials, really at like the stage where they're just checking the safety of these drugs and making sure that somebody can take them without, you know, getting really sick or, God forbid, dying or something like that. But even when they're doing, like, those safety checks, they do start to collect, like, qualitative data about, you know,

well, are we starting to see any effects? And some of the preliminary results from some of these Tao targeting treatments that are in the works have looked pretty promising. And so that's encouraging, obviously. It's possible that we're moving towards a future where, not unlike cancer treatment, there's not just like one drug for Alzheimer's disease, but maybe you take a combination of different things that work on different mechanisms for the disease. And, you know, the collective, cumulative effect is that, you know, it stops the progression or even reverses it. And so the hope is that, you know, five, ten years from now, we've got a much more robust suite of treatments that can help somebody who's been diagnosed with Alzheimer's.

I mean, five, ten years from now sounds nice, but is there anything else that's in the cocktail now that people are discovering could be promising for Alzheimer's? So there are also, yes, like drugs that millions of people are taking right now for other reasons that might also be able to help with Alzheimer's disease. And GLP-1s in particular are the big one. No way.

Yeah, I know. These drugs that it seems like every day you see some new headline about this miraculous thing that they can do. weight loss, smoking, my poker addiction, and? And it might prevent dementia down the road. But, I mean, if you step back and think about it, the theory does make some sense. Like I said before, scientists increasingly think there's association between your vascular

health and your cognitive health, especially as you age. And what do these GLP1 drugs do? They help people lose weight. Losing weight helps to, you know, lower your blood pressure. lowers your risk of vascular problems, whether it's heart disease or pulmonary disease or stroke or something like that. And, you know, so if more and more people take these, they take them earlier in life, they lose weight, they keep it off, they don't develop these heart or vascular problems, it does make some sense that that may also reduce their risk of developing Alzheimer's disease.

Now, it's still sort of theoretical, but the Alzheimer's Association is putting $100 million behind some research projects to investigate this possible link. And so, again, we may learn five, ten years from now as millions of people are now in these GLP1 drugs, maybe we start to see Alzheimer's less often. And that would be another reason to be optimistic that, you know, the future for this disease is looking brighter. Okay, so we got some treatments. We have potentially preventative measures.

How about reversing it? Is that still a pie in the sky? It's out of reach for now. Certainly some of the scientists that I've talked to have said, like, in theory, it should be possible. Like, your brain is really resilient. It's really good at rebuilding itself if you give it the chance. So it seems like it should be possible to certainly, like, stop the progression of the disease eventually and maybe ultimately reverse it. Now, there has been some really intriguing, but also mysterious developments around reversing Alzheimer's. Not, you know, from scientists based out of the United States, but from scientists in China. All right, so today let's go into talking about a probably new treatment for Alzheimer's disease. People may have seen or may not have seen that there have been videos of these patients who underwent an experimental surgery, and the before and after of these videos is incredible. And the before you've got somebody who clearly has Alzheimer's disease, doesn't recognize,

their loved ones, has trouble with their train of thought. And then the after videos are like, it's like they're a completely different person. Zsuzzo, what's your name? You know, Zhou Shiz. Oh, where's where? They recognize their loved ones, they're talking articulately. And so that has, as you can imagine, generated a lot of excitement, also a fair bit, of skepticism. Jinks! I owe you a Coke. You owe me a Coke. Are they real? Are these

videos real? Do we know? Are they great videos? We don't, I don't, what we don't know for sure is, like, we don't know for sure if they're real or not. So the way this, but what's intriguing about this surgery is the theory of it, at least to me as like a layperson, makes some sense. The gist of this surgery is the surgeons create a drain in the patient's brain and the drain is supposed to help the brain get rid of these amyloid and tau proteins that we think are associated with Alzheimer's disease. So, like, hypothetical level, it makes some sense. Now, and scientists in the United States and Europe and elsewhere have been intrigued enough about these videos and the findings that have been reported in academic journals to set up

their own studies to try to replicate these findings. Now, I, it's just, it's a crazy story, because this scientist in China, who pioneered this idea, has actually been arrested by the Chinese government. And as I understand it, he's currently in detention. For what? The reporting I saw was these seem to be like kind of flimsy charges of insurance fraud. The Chinese government has also tried to ban the surgery, at least outside of like clinical trial settings. So that's, I mean, that's obviously sort of complicated the story a little bit. But nevertheless, you do have scientists in the U.S. and outside of China who are like, well, we at least want to try this for ourselves and see if it works. It does feel like it's something that could get people's hopes

up who have been waiting for this for decades. Exactly. I mean, I think this is like the holy grail. Can we find a way, whether through surgery or through pharmaceuticals, to actually reverse these symptoms and, like, restore the person to who they were before? for Alzheimer's took over. Because that's the thing that, like, I think everybody recognizes, but is worth emphasizing as, like, as one doctor put it to me,

and I've never forgot it, like Alzheimer's is a disease unlike any other because it robs you of your identity. And so to be able to restore people's identity through whatever means, like that is the goal that all of these scientists are chasing. That was Dylan Scott,

who writes for Vox, Miles Brian, Amina al-Alsati, Avi Shai Artsy, Hadi-Mawadi, David Tattishore, and Bridger Duggan make today explained for Vox.

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