Charles Piller
speaker
984 appearances
4 recordings
4 series
first heard Mar 2025
last heard 17 Apr
Charles Piller’s voice in public audio — every appearance, attributed to the second.
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and Jay Bhattacharya, who is the new National Institutes of Health director, where they have referred to my reporting as a way of describing how critical they are of the research realm, particularly in Alzheimer's research. And it's an awkward position for me for this reason. I believe that they're right to challenge some of that research, to call out some of the problems in it. And
I wouldn't have written about it if I didn't believe it was important. Of course, I think it's important and I appreciate their interest in it. What I do not appreciate is the slash and burn approach to removing huge portions of Alzheimer's research and other forms of research from the NIH. and from the capacity of FDA to evaluate new drugs.
For all their flaws, these agencies have done generally a very good job in many ways. Even though I'm very critical of them, I want to see them strengthened and not greatly and radically reduced.
So I just want to make it clear that I think you can have a different position and still support some of what's going on and be critical of a lot of the other things that are happening with the new administration.
You have a way of capturing my long answer in a few key words, Dylan. Thank you for doing that.
Sure. So perhaps it would be good if I went back to the beginning of how I started to do my reporting for this book and why. And it all began when I got connected with a young professor at Vanderbilt University, a guy by the name of Matthew Schrag. who was a guy who had been looking into a particular Alzheimer's drug called Simufilam from a company called Cassava Sciences.
Now that drug crashed and burned, is no longer being even thought about as a possible remedy for Alzheimer's. It's a long story I tell in the book, but I'm going to pause away from that for now and talk about why that led to this bigger set of issues. And that's because
Schrag, who is himself a neuroscientist who researches in a lab some of the potential causes of Alzheimer's disease, and also somebody who treats Alzheimer's patients, because he's also a physician who is a neurologist who has patients who have the disease. And he... had over the many months begun to hone his ability to see potential doctoring and scientific images.
And what I mean by that is he could look at images, say, of brain tissue, magnifications of brain tissue, and be able to look at them and see the possibility that someone had used a program like Photoshop to move some things around or to obscure certain elements of the image or to copy elements and clone them within an image
all to accentuate a point that was being made for a scientific paper, but to do so improperly in a way that is essentially a kind of scientific cheating. And because he had developed the talent for seeing these things from looking at this, initially looking at the science behind this drug, semufilam, he was looking more broadly to expand his ability to do this.
And he, in a way, kind of just by accident ran across one of the seminal studies in the history of Alzheimer's disease. Now, this was a study done in 2006 at the University of Minnesota. And what this study did, if I could just
use a few, a little bit of scientific explanation to bring this experiment to life for listeners a little bit, is that it involved a group that was using genetically engineered mice to produce copious amounts of a protein that deposits in their brains. This protein is called amyloid.
And it is thought by many, many, many people to be the linchpin of Alzheimer's disease, the thing that kicks off a series of biochemical effects in the brain. that leads to cell death in the brain and ultimately to dementia.
And so what he was doing when he kind of stumbled on the study and was looking at its images is that he realized that there were some big questions about whether these images were improperly changed. And so I remember the first conversation that Schrag and I had about the images in this seminal paper that had appeared in the journal Nature.
Now, you remember I said that the journal I work for, Science, is one of the preeminent scientific journals. Nature also is kind of its counterpart. Science and Nature are two journals that are often thought of in the same light as being the most important general science journals out there. And so to get an article into Nature means that you're really hitting
something really important and potentially could have a lot of influence. And this study had enormous influence. It was one of the most cited and discussed studies in Alzheimer's disease for a very long time. And The way the experiment went was this. They extracted these proteins from the brains of these genetically engineered mice.
They refined just one little segment of the protein, something they called amyloid beta star 56, their star protein. They injected it into rats, and rats began to show the apparent symptoms of memory loss that they compared to memory loss of Alzheimer's disease.
So what you had was the first kind of cause-effector relationship of a particular substance towards Alzheimer's disease, albeit in animals, but still something that really inspired the science. Now, Why was it so important? Why was it so pivotal? If you don't mind, Dylan, what I'd like to do is go back more than 100 years to tell kind of the story of the disease. How did we get here?
Why was this a meaningful part of the scientific picture? So the reason is that Alzheimer's disease was first described in 1906 by the German scientist Alzheimer, namesake of the disease. And it involved... When he did... an examination of brain tissue from one of his patients who had died with terrible dementia. And this brain tissue showed these two kinds of really obvious proteins.
One was this amyloid protein that I mentioned before, the so-called sticky plaques that listeners may be familiar with that are regarded as a classic sign of the disease. And another protein that is called tau, which is called the tangles because it looks like kind of tangled string and it resides within the nerve cells of the brain.
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