Good news about Alzheimer’s

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 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. Ryan Reynolds here for Mint Mobile with your summer price forecast. Now unfortunately we're seeing rising costs across the country with possibility that big wireless hates you 100%. Now over here at Mint Mobile we're seeing sunny skies and dropping prices every plan to just $15 a month. 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To explain Sean Rama's firm something like seven million Americans have all simers 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, immunotherapies, stem cell, transplants. The list goes on but all simers 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 ask science magazine investigative journalist Charles Piller why that is so in order to understand the answer to that let me take you back actually more than a hundred years to the when all simers was named its namesake scientist Alois 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 plaques 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 had 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 to 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 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 under 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 this theory which is a beautiful theory of the idea 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 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 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 experiment 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 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 were been attacking things maybe in a 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 amyloid proteins that float around in the cerebrospinal fluid that bathes 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 development 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 cross 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 Schragg at Vanderbilt University he encountered this seminal report the seminal study that appeared in nature a journal that is one of the most eminent and important scientific journal journals. And what he looked at is the scientific images that were described in this experiment where they found this particular type of family 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 doctrine. 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 that purported to show the great advance of amyloid beta star 56 was based on apparently doctored images. And eventually, the doctrine 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 billions of dollars have 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 par of things that would at least stop the disease and its tracks, I think we have caused 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 have to understand the bad to appreciate the good that's coming next on today's split. So both of the charity comes from China. 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 blush? 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 China comes in. China 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. China, 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 America's number one choice for banking at the chime.com/explained that is chime.com/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 Chime's bank partners, qualifying direct deposits required. Terms and limits apply. Go to chime.com/disclosures for details. Hey there, it's Sue Bird. You know the drill. Another week, another new episode of Birds Eye View. This week I'm thrilled to be joined by Australia's most notable women's basketball player and my former Seattle Storm teammate, Lauren Jackson. She talks about the pros and cons of going pro at 16, the Opel's legendary FIBA World Cup run in 2006, and how her role on a team differs between international tournaments and the WMBA. Plus in Sue's view, I answer your questions about the Yukon documentary that came out. Make sure to check out Birds Eye View on YouTube and wherever you get your podcasts. After years of rumors, Apple finally launched a folding iPhone. The iPhone Duo starts at $2,000, making it Apple's most expensive phone ever. It's Apple's bold attempt at proving that folding phones are finally worth your attention. This week on the Vergecast, we went live from Apple Park with our first look at all the new gadgets. Plus, Lauren Feiner explores the tech behind the two-hour marathon, and the story of how big tech set the agenda for our students are taught to code. Check out the Vergecast wherever you get your podcasts. 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 him 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 to address and so there's been a lot a lot of investment in manpower and money into detecting Alzheimer's disease and coming up with like blood test 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 like 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 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 Lecanomab and Danomab we are our memories so I want to hold on to them as long as I can and anti-hammaloid 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 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 that 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 like 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 to 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 tau 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 the collective cumulative effect is that it stops the progression or even reverses it. And so the hope is that five, 10 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, 10 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 ones 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 it might prevent dementia down the road. But I mean, if you stop, 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 GLP one drugs do? They help people lose weight, losing weight helps to 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 association is putting $100 million behind some research projects to investigate this possible link. And so, again, we may learn five, 10 years from now as millions of people are now in these GLP one 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 behind the sky? It's out of reach for now. Certainly some of the scientists that I've talked to 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. So let's look here. You may have seen or may not have seen that there have been videos of these patients who underwent an experimental surgery and, you know, the before and after of these videos is incredible. And the before you've got like 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. 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. Skepticism? Jinx! 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, 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 lay person, makes some sense. Based the gist of this surgery is the, the surgeons create a drain in the patient's brain and the brain, the drain is supposed to help the brain get rid of these amyloid and towel 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 the scientists 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 think that's obviously sort of complicated the story a little bit, but nevertheless, you do have scientists in the US 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 Alzheimer's took over? 'Cause that's the thing that like, I think everybody recognizes, but as worth emphasizing is 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. (gentle music) (gentle music) - That was Dylan Scott who writes for Vox, Miles Bryan, Amina Alsaadi, Avishai Artsy, Hadi Mahwagdi, David Tatashore, and Bridger Dungan make today's explain for Vox. (gentle music) (gentle music)