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Reporter: Do you remember my name?
Carol: No.
[MUSIC IN]
HOST: In this 2018 clip from 60 minutes, a woman is dealing with one of the most troubling diseases of old age: Alzheimer's.
Reporter: “What’s this called? What I’m wearing on my wrist? What’s the name of that?
Carol: “Ummmm… I don’t know”
Reporter: “It’s a wristwatch”
Carol: “Oh, yeah!”
Reporter: “Does that sound familiar?”
Carol: “Yeah.”
HOST: Alzheimer's disease is the most common form of dementia. Memory by memory, it erases everything we know, including our sense of who we are. Eventually, it can rob us of our ability to walk, talk, and care for ourselves.
The numbers tell a grim story. Every year over half a million Americans are diagnosed with dementia – most will be Alzheimer's cases. and over 100,000 Americans die of Alzheimer's each year, which makes it the seventh leading cause of death in the United States.
The crisis is only going to get worse. As more people live into their seventies and beyond, the population of people with Alzheimer's will grow.
So it’s no surprise that scientists are furiously searching for a cure, and have been for a long time. between drug companies and the U.S. government, billions of dollars have been spent on Alzheimer's research in just the last 30 years. But despite all that time and money, we still don’t have a reliable treatment for the disease, let alone a cure.
Why haven’t we made more progress against a disease we’ve known about for more than a century? And do we even understand how it works? Or have we been heading down the wrong path since the very beginning?
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I'm Carl Zimmer. And in this episode of the world as you’ll know it: the future of aging, we’re looking at the state of Alzheimer's research — where we are, how we got here, and where we go now?
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In order to understand why we’re still searching for an Alzheimer's cure, you have to go back to the beginning. and one of the best people to take us there is Dr. Karl Herrup, a neurobiologist at the University of Pittsburgh. A few years ago he published a book called: How Not to Study a Disease: the Story of Alzheimer's.
Karl Herrup: So let’s go back to 1906. Alois Alzheimer, an up and coming psychiatrist in Germany, is fascinated with the idea that the structure of the brain dictates its function. And that was a very forward looking idea for its time.
HOST: Dr. Alzheimer was working at the Frankfurt psychiatric hospital when a woman named Auguste Deter was admitted. She was fifty years old, and she had become paranoid. She accused her husband of adultery. She was convinced someone was trying to kill her. She would compulsively move things around the house and hide them for no reason.
Eventually Auguste's family could no longer care for her. They moved her to the frankfurt hospital and after five years, she died there.
Dr. Alzheimer was so struck by Auguste's case that he had her brain preserved. He thought if he could study her brain, he might find the source of her illness.
Carl Zimmer: So when he, when he looks through the microscope, take us through what he was seeing at that time.
Karl Herrup: I mean, we call them deposits, but they're just piles of goo in the brain. And then in addition, these ghosts of dead neurons, which he described as military tangles because they looked like just twisted strands of wire.
HOST: Dr. Alzheimer wrote a paper about what he saw in Auguste's brain.
KARL HERRUP: And he said, I don't see these normally. They are abnormal. Auguste's behavior was abnormal. Therefore, those plaques and tangles must have caused the behavior.
Now, that's a perfectly good hypothesis, but an equally valid hypothesis from the data that Alzheimer had would be to say, no, no, no, no, no, no. The disease, the dementia, the behavior itself was what led to the deposits. They were symptoms rather than causes. And there's no way to untangle that, given the data that Alzheimer had. But he was perfectly entitled. In fact, it was a forward looking paper to put out this idea that the plaques and tangles caused the dementia.
HOST: Soon after the paper was published, Auguste Deter’s condition got a name: Alzheimer's disease. For decades, doctors believed it was a peculiar form of early dementia caused by plaques and tangles in the brains of middle-aged people.
But by the 1960s, pathologists started finding those plaques and tangles in a lot of old people with dementia. This transformed Alzheimer's from a niche disease to a widespread threat.
Carl Zimmer: So Alzheimer's goes from being this very rare condition that someone like Auguste Deter gets when she's in her 50s to something that a substantial number of people are getting who are over 65 in addition.
Karl Herrup: That's correct.
HOST: In 1974, the US government set up a new research center, the national institute on aging. It deployed an army of scientists to use the latest technologies to make sense of Alzheimer's. And, according to Herrup, this new generation of Alzheimer's researchers did something that would set the stage for the next 60 years: they took Dr. Alzheimer's original hypothesis as fact.
KARL HERRUP: What they basically decided was that we see plaques and tangles in dementia, even if it occurs later. Therefore, all of this dementia must have the same cause. And they ran with it and were hugely successful.
HOST: Starting in the 1980s, researchers made significant progress in understanding Alzheimer's. For one thing, they discovered what plaques are made of. Brain cells sometimes expel a defective fragment of a protein. That fragment is called amyloid beta. and amyloid beta sticks together, forming clumps between brain cells. That's what Dr. Alzheimer first saw – what we now know as a plaque.
These discoveries allowed scientists to develop theories about the cause of Alzheimer's on a molecular level. By the 1990s, amyloid beta emerged as the prime suspect. and one explanation for how it wreaked its damage began to dominate the field.
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It said that Alzheimer's starts when amyloid beta begins to clump into those plaques. That triggers all sorts of changes, including the death of neurons. Gradually, according to this explanation, amyloid beta destroys the brain, causing the devastating behavioral symptoms of Alzheimer's.
Scientists called this explanation the amyloid cascade hypothesis.
Karl Herrup: Perfectly plausible hypothesis. It fit all the facts.
Carl Zimmer: And I guess if amyloid was the cause of dementia, then that gave you a very clear target to cure Alzheimer's.
Karl Herrup: That is correct….
HOST: At the time that amyloid was becoming a central target of Alzheimer's research, Herrup was just entering the field. But when he looked at the amyloid cascade hypothesis, he was skeptical. If amyloid was the key to Alzheimer's, then you’d expect that everyone with amyloid build up in their brains would have Alzheimer's, right? Turns out, that’s not the case.
Karl Herrup: If you look in the brains of healthy people, that is to say, elderly people with no cognitive deficits, you know, no symptoms at all, 30% of them, they’ll have deposits of amyloid that could be diagnosed as Alzheimer's disease.
HOST: Herrup brought his concerns to the Alzheimer's experts he was working with. He told them he wanted to study other potential causes of the disease.
Karl Herrup: The response at that time was to kind of puff up their chest, cluck their tongue and say, son, if you're not studying amyloid, you're not studying Alzheimer's disease.
Carl Zimmer: Wow they actually said that to you?
Karl Herrup: Oh yea, it was a meeting I will never forget.
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Karl Herrup: So you can imagine what an outlier I was in being skeptical and questioning of a field that was just getting excited about how we had pretty much figured out this disease and would cure it within just a few years.
HOST: And for a few years, things did look promising. In the late ‘90s, researchers at a company called Elan pharmaceuticals engineered mice to make amyloid plaques in their brains. and, lo and behold, the plaques damaged their brain cells. Just what you’d expect from the amyloid cascade hypothesis.
Then the scientists at elan took the next step. They gave the mice a vaccine that trained their immune system to attack amyloid.
And it worked.
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HOST: If a mouse got the vaccine when it was young, it didn’t go on to develop plaques. If the scientists gave the vaccine to old mice that already had plaques, their immune system attacked them.
Karl Herrup: The plaques in the mouse brain disappeared and so did the behavioral abnormalities. And even I, as the skeptic was saying at the time, it would be almost irresponsible not to take this into people and see if it had the same effect.
HOST: So Elan Pharmaceuticals launched a study on people. But…people are not mice.
Karl Herrup: Human clinical trials were done and almost immediately had to be halted because it turns out when you make antibodies against amyloid, you induce an encephalitis.
HOST: Encephalitis is an acute inflammation of the brain and its membranes. All the volunteers who developed encephalitis got better. But the vaccine was clearly too risky to use on patients. and the researchers couldn’t be sure whether the vaccine slowed down the memory loss and other symptoms of Alzheimer's. Elan abandoned the vaccine trial in 2002.
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Charles Piller: This was a very, very difficult state of affairs for the proponents of the amyloid hypothesis. They felt discouraged. Many people in the field were starting to think, have we bet on the wrong idea here?
My name is Charles Piller, and I'm an investigative journalist with Science magazine and the author of Doctored, a new book about Alzheimer's research.
HOST: Charles Piller has spent his career investigating public safety issues in tech and science. In 2021, he turned his eye towards Alzheimer's.
Pillar started investigating a prominent paper that came out right during that tough time for the amyloid cascade hypothesis.
Charles Piller: Something happened in 2006 that profoundly affected the field. And this was a brilliant experiment coming from two scientists, primarily at the University of Minnesota, Karen Ashe and Sylvan Lesne. These two scientists did something very clever. They were able to isolate from the brains of genetically altered mice a particular kind of amyloid protein that had the clever name amyloid beta star 56, a very catchy name. And they took this star 56 protein and purified it and then injected it into rats. And the rats then seemed to exhibit the symptoms of Alzheimer's disease, such as memory loss.
HOST: It looked like star 56 might be the very essence of Alzheimer's. This specific kind of amyloid was all it took to trigger symptoms — even if you moved it from the brain of a mouse to the brain of a rat.
Piller: The field took notice. It was described by many of the top names in the field as fundamentally supporting their own ideas about the importance of the amyloid hypothesis. And consequently, it had become one of the most cited basic research studies on Alzheimer's in decades.
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HOST: While Ashe and Lesne were publishing their results, drug developers were searching for new ways to treat Alzheimer's based on the amyloid cascade hypothesis – ones that wouldn’t cause brain swelling.
A number of companies created antibodies against amyloids. To test them, they injected the antibodies into people with Alzheimer's, believing that the antibodies would zero in on plaques and prompt the immune system to wipe them out, leading to an improvement in symptoms.
At least, that was the hope. The reality proved a lot messier.
The trials dragged on for years. In 2021, the FDA finally approved the first antibody drug, called aducanumab. It was put on the market, with a prescription costing a whopping $56,000 per year.
But the approval was not without controversy. Not a single one of the FDA advisors who reviewed the drug recommended it for approval.
They said the clinical trials hadn’t demonstrated any significant benefit to patients. And that the results of the trials were contradictory.
The FDA ignored their advice, and approved it anyway. Several of the advisors for the drug trial resigned in protest.
That was in June of 2021. It wouldn't be long before Charles Piller uncovered a different controversy: not just a disagreement regarding efficacy, but a full-blown scandal inside the field of Alzheimer's research.
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In recent years, independent watchdogs have begun to find misconduct in scientific papers from many different branches of medicine. Some scientists have fabricated data and doctored images to make their results look more impressive. In fields ranging from cancer to cardiology to psychology, journals have retracted thousands of papers.
In late 2021, Piller got a tip about one of these misconduct cases. He learned that one of these watchdogs, a neuroscientist at Vanderbilt University named Dr. Matthew Schrag, had been investigating a new Alzheimer's drug from a company called cassava sciences.
Charles Piller The allegations made about their work involved the falsification of images and their basic science behind a drug they developed called SIMUFILAM, which was described as being a remedy, perhaps even a cure for Alzheimer's disease.
HOST: Schrag noticed irregularities in some of the images supporting how the drug was supposed to work – essentially, they looked photoshopped. The images showed how certain molecules in the drug affected different parts of the brain. Pretty important for a treatment for a brain disease.
The drug was already in clinical trials when Schrag discovered these signs of fraud. He wrote up a report and contacted the national institutes of health, alerting them that cassava was testing a drug on humans based on potentially fabricated data.
Schrag had done his part, and now he could let the authorities take it from their end of story.
Charles Piller: Actually, this was just the beginning
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HOST: While investigating cassava sciences, Schrag began testing some new techniques for finding and examining potentially manipulated images. He wanted to try them on some fresh examples – something unrelated to cassava. so he picked up the Lesne/Ashe study zeroing in on star 56.
Charles Piller: He examined this study from 2006 in Nature, this seminal study that had been so important in the field and found, to his surprise, that some of the most important images that proved out the basic premise of the study were themselves apparently based on manipulated, altered images.
HOST: Piller checked Schrag's findings with a number of other experts. They independently confirmed that the images had been altered, and in the summer of 2022, Piller went public with the findings that this influential paper seemed to be based on doctored data.
Carl Zimmer: What happened once that came out. What was the impact?
Charles Piller: The story hit the field very hard. It was immediately the subject of global news headlines, including in Europe, Asia, South America, the United States. And I think in the field it caused a real shudder of recognition.
HOST: The Lesne/Ashe paper might have been the most prominent Alzheimer's study marred by image fraud, but it was far from the only one. Schrag learned that even his own undergraduate adviser had manipulated images for dozens of papers. Including ones he and Schrag had published together. Schrag has since retracted several of those papers.
The fallout from these investigations has continued for years. Take the Cassava Sciences drug. The scientist who led much of the work on the drug has been indicted for fraud for doctoring images. The CEO of Cassava Sciences and its head scientist were forced out of the company and were fined tens of thousands of dollars. And in 2024, the company discontinued development of its Alzheimer's drug entirely, after it failed in clinical trials.
And then there is the star 56 paper from Karen Ashe and Sylvain Lesne. Ashe and most of her co-authors concluded that image doctoring had occurred and retracted the paper in 2024.
But Lesne stood by the paper. As a result of Piller and Schrag’s work, the University of Minnesota, where Lesne and Ashe had done their research, investigated Lesnar for two and a half years. The university asked for four of his other papers to be retracted. and in early 2025, Lesne resigned from his position.
Carl Zimmer: After looking into all these different cases around Alzheimer's. I mean, do you have any insight into why people would do this? I mean, fabricating results in any kind of science is bad enough. But this is Alzheimer's. These are studies that could lead to drugs that might or might not work to help families in incredible pain and suffering. Why do people do this?
When a single dominant idea takes hold in the field, it becomes easier to write papers and to continue to reinforce that idea because it becomes the conventional wisdom. And what we've seen in Alzheimer's disease and I have found in my work for doctored is that a huge number of other Alzheimer's studies have been altered, the images have been altered and has skewed research thinking in the field, and most of them have been associated with the amyloid hypothesis, in part because there's a lot of complacency among journals, among peer reviewers and other scientists in the field. If something supports an idea that everyone believes, it becomes easier to create ideas that support it, that are indeed false.
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HOST: I asked Karl Herrup for his take on these revelations.
Carl Zimmer: There have been a series of reports in the past couple of years about some scandals in the field. And I just wanted to get your view on how this all happened and what you think the effect on the field is.
Karl Herrup: This may come as a shock, but we scientists are human beings and we have egos and some of us have an unjustified certainty that we know how a disease works. And if that arrogance is sufficiently great, you are so confident that when you look at a Western blot or an image of a microscope slide that doesn't fit your theory? Well, the slide must be wrong. So it's okay if I do a little Photoshop work and make it look like what I know is the right answer?
It's a problem that's certainly not unique to Alzheimer's disease, but it, somehow our field seems to have attracted our fair share of those oversized egos.
HOST: The Alzheimer's field is taking steps to prevent misconduct. Journal editors are using new tools to discover fabricated images. Scientists now have to permanently archive their data so that it can be reviewed later.
But even if these scandals end, the controversy over current Alzheimer's drugs is far from over.
Since the FDA approved aducanumab in 2021, two additional amyloid clearing drugs have also been approved. They work in much the same way, using antibodies that attack amyloid — and like aducanumab, the assumption behind them is that if you can get rid of the amyloid, you can stop Alzheimer's disease.
But all three amyloid-clearing drugs – Aducanamab, Lecanamab and Donanemab – cost tens of thousands of dollars a year. If governments have to pay for everyone with Alzheimer's to receive them, their health budgets will go up in smoke.
Making matters worse, all three drugs have been linked to a small number of deaths in clinical trials. Those deaths were not reported until after the drugs were approved, and even then only because of investigative reporting and independent reviews – not because the drugmakers disclosed them.
In 2024 Aducanumab was pulled from the market by its manufacturer, a move the company claims was not related to safety or efficacy.
The debate about efficacy continues. Critics like Herrup argue that the new drugs don’t help patients improve; they only help them decline a little more slowly.
Karl Herrup Everyone in the clinical trial, both people on antibody and people on placebo got worse during the 18 months of the trial. No one got better. Treatment or no treatment, I look at that data and I say, that doesn't pass the grandmother test, which is, would I want my grandmother to have this happen to her brain. I say no, given the very small benefit. So even if we accept that there is a benefit and I'm not entirely still not entirely sure that there is, the risks are too substantial for the tiny benefit that is offered.
HOST: But other Alzheimer's experts have a different take.
Donna Wilcock: With both drugs, the benefit was around 21 % slowing decline. When we extrapolate out this data and say, this could be three years of living in their own home and having a reasonable quality of life. And I think that means a lot to patients.
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Donna Wilcock: Yes, so my name is Donna Wilcock. I am a professor of neurology at Indiana University School of Medicine. I also lead the Center for Neurodegenerative Disorders.
HOST: Donna Wilcock has been studying Alzheimer's disease and other forms of dementia since the 1990s. She is also the editor-in-chief of Alzheimer's and Dementia, which is the official journal of the Alzheimer's association. And she thinks the new drugs are a promising start. Data from trials suggest that the drugs make it easier for people to sustain what scientists call activities of daily living.
Donna Wilcock: We're talking about things we do every day, brushing our teeth, bathing, clothing, remembering to take medications, eating breakfast, lunch and dinner. These are all activities of daily living. And the benefit on a scale measuring activities of daily living was closer to a 35% slowing of decline. Cognition matters, obviously memory matters to people, but for quality of life, I think activities of daily living are what people really care about.
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Carl Zimmer: So how much of a role does amyloid play in your work in terms of trying to cure Alzheimer's?
Donna Wilcock: So when we think about the role of amyloid in Alzheimer's, I think our ideas and our hypotheses have evolved. When I came into the field, which shockingly is 25 years ago now, we were working very much on a very basic amyloid hypothesis, which was that amyloid was the initiating factor that would then drive the formation of tangles. The tangles would cause the neurons to die, and it's the neurons dying that causes the cognitive impairment. If you'd have approached a lot of scientists and said, hey, we have a drug that completely clears the amyloid from the brain, I think a lot would have thought that would be the cure. As time has gone on and as our science has progressed, and especially in the last 10 years, we've had an explosion of science, technology that's allowed us to study things in different ways. We’ve learned that amyloid is certainly one of the earliest events that happen in the disease. But the progression from amyloid is a lot more nuanced. And so I do still believe that the amyloid hypothesis is correct with many modifications from where it was 25 years ago.
HOST: To Wilcock, Amyloid is one step in a transformation of the brain that takes decades.
Donna Wilcock: We know from some beautiful studies that have been done that everybody, even my kids who are teenagers, everybody is making beta amyloid in their brain. We don't know why. We don't know what process, what normal biological process is causing this to happen, but we all make it. The thing is we all also clear it effectively. Usually either into our blood or into our spinal fluid, we get rid of it. The brain has a garbage disposal system that gets rid of all this junk.
HOST: That garbage disposal system includes special immune cells in the brain, called microglia. It's possible that microglia start to fail at their job. and as a result, amyloid beta builds up in the brain.
Wilcock says that chronic inflammation could drive microglia to fail. That inflammation might happen somewhere else in the body—like arthritis in the joints.
Donna Wilcock: Even though the symptoms of those inflammatory conditions are systemic, you know, joint pain, gut dysfunction, those proteins that are made by the inflammation also get to the brain and probably modify the microglia and probably modify how effectively we can get rid of the junk from our brain. We have epidemiology studies that have looked at this retrospectively. So they've looked at people who have been on drugs for rheumatoid arthritis for a long period of time.
And it appears like there is some protection from that. Unfortunately, the immune system is incredibly complex. You know, I mean, immunologists could probably take up this whole room that I'm sitting in writing out all the different immune pathways that exist.
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HOST: Wilcock says the buildup of plaques has something to do with how Alzheimer's disease starts to kill neurons. One possibility is that it spurs the formation of the tangles inside neurons. But once tangles start to form, getting rid of plaques may not stop Alzheimer's. And sometimes the build up of amyloid doesn’t lead to Alzheimer's at all.
Carl Zimmer: What about when skeptics will point to people who have amyloid in the brain and don't show symptoms of Alzheimer's? A substantial fraction of people, even in their 60s, have amyloid in their brain and they don't show the diagnosis of Alzheimer's and how they're acting and so on. And so that's led to questions about how important amyloid actually is to Alzheimer's.
Donna Wilcock: Yeah, and it's a common argument that is used against the amyloid hypothesis. You're very correct. There are people that come to autopsy that we look at that have a lot of amyloid and died perfectly cognitively normal. You know the true explanation for that, I think, we don't know, is the answer. But we have a lot of hypotheses as to why that would be. And one…
Carl Zimmer: Do you have a favorite one?
Donna Wilcock: I have a favorite one and that is resilience.
HOST: Wilcock says that some people may be able to compensate for the damage caused by inflammation or amyloid or tangles. Maybe they are lucky and inherited genes that protect their brains. or maybe their experiences earlier in life gave them the defenses to withstand Alzheimer's.
If that's true, then we can all take steps when we’re younger to slow the progression of Alzheimer's later in life. Some studies suggest that education, exercise and a healthy diet may help tamp down inflammation and other triggers for Alzheimer's.
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HOST: Lifestyle changes might reduce the rates of Alzheimer's disease decades from now. But the Alzheimer's crisis is already here.
Carl Zimmer: What's gonna happen if we don't make some big strides on Alzheimer's?
Donna Wilcock: You know, it's going to bankrupt families. It's going to bankrupt health care systems. Millions of people are going to be in nursing homes. We're going to have millions and millions of individuals who are at the prime of their life--people my age, people 40s, 50s — who are quitting work to look after their parent because they can't afford nursing home care. And if we lose a workforce because they're caring for elderly parents, that's another economic impact that I think is underestimated.
I mean, this used to seem like a long way off to me, and now it's imminent. Right, we can't have another 25 years to get one more drug to the clinic. We have to be having a push as quickly as we can.
HOST: Wilcock is optimistic that she and others can meet that challenge. Some researchers are tailoring amyloid antibody drugs so that they are less likely to damage blood vessels and cause bleeding. Meanwhile, other researchers are working on drugs that attack the tangles inside of neurons. And there are even trials of drugs similar to Ozempic that might reduce inflammation in the brain.
Wilcock acknowledges there’s been a hyperfocus on the amyloid cascade hypothesis. but she argues that long-term support for Alzheimer's research has allowed scientists to pursue different avenues for a cure.
Donna Wilcock: With increased funding, with increased research and increased technology, we understand so much more about this disease now. We know that amyloid is not gonna be the only target. And the funding for trials and even when you look at the portfolios for the different drug companies, there's not a lot of amyloid in there anymore, right?
Carl Zimmer: Mmhmm.
Donna Wilcock: We're looking at other things. And mostly because we've been able to check amyloid off the list.
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Carl Zimmer: I’m curious, when you started in the Alzheimer's field over a quarter of a century ago, what did the future look like to you?
Donna Wilcock: At that time, I think we as a field, and myself, thought it was a simpler problem and that if we could get rid of that amyloid, man, we'd be made in the shade. And I remember, it was probably the year 2000, going to a conference and someone was asked, you know, when do you think we'll have a treatment? And the answer was five years. And in 2005, I heard the same question being asked and the same answer was given. And in five years, we'll have something in five years. I've been hearing the five years for 25 years. And it's this, well, last year when we could say we have something, but it's not a cure. It's not a cure. It's a start. I'm not gonna take any credit for saying this, but at a conference someone said, it's not the beginning of the end. It's the end of the beginning.
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HOST: On the next episode of The World As You’ll Know It: The Future of Aging.
Dena Dubal: There are certainly cultural, behavioral, environmental aspects to why women do live longer than men. But given how extensive and pervasive this is and the fact that we see this in the animal kingdom. It tells us there's something biological going on.
Virginia Zarulli: These people moving there faced what we call a mortality shock. It was very high mortality for both sexes, of course, but at all ages women were surviving a little better than men.
Carl Zimmer: Females still would end up with this lower mortality rate even in times of crisis.
Virginia Zarulli: Yes.
Dena Dubal: If we can understand what makes one sex more resilient, then we can apply that new knowledge to both men and women.
CREDITS:
HOST: The World As You’ll Know It is brought to you by Aventine, a non-profit research institute creating and sharing work that explores how today’s decisions could affect the future. The views expressed don’t necessarily reflect those of Aventine, its employees or affiliates.
For a transcript of the episode and more resources related to what you've just heard, please visit aventine dot org slash podcast.
Danielle Mattoon is the Executive Director at Aventine. Bruce Headlam is the Editorial Director at Aventine.
Our Producer is Emerald O’Brien. Our Associate Producer is Marialexa Kavanaugh.
Our Editor is Joel Lovell. Kamilah Kashanie is our Managing Producer.
Original music by Davy Sumner with additional music from epidemic sound.
This episode was mixed by Marina Paiz.
Our head of sound and engineering is Raj Makhija. Our Senior Recording Engineers are Marina Paiz and Pedro Alvira.
Fact Checking by Will Tavlin.
Music licensing by Extreme Music and Epidemic Sound.
Our executive producer is Asha Saluja.
I'm your host, Carl Zimmer.
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