Tarek Pasch, Tarik, 113 Videos discussed on Here and Now
I'm Ira Plato. The brain of a person with Alzheimer's disease has a few Hallmark traits. First, there's a build up of plaques of proteins called amyloid Beta. Second or tangles of another protein called Tau within individual neurons, and the third is inflammation. And while researchers have long thought the inflammation was a byproduct of the disease itself There is a growing hypothesis that it may be something else a driver of the disease progression that would help explain why researchers have found people whose brains are full of tau tangles and amyloid plaques, but with no outward symptoms of disease. Research on animals has supported this theory but finding the same evidence in human brains. Well, that's a lot harder. But now a team of scientists thinks they have it time lapsed images of patient brains showing tau tangles and inflammation spreading through the brain in the exact same pattern. Here to explain is the first author of that research. Dr Tarek Pasch. Wow. He is an assistant professor of psychiatry and neurology at the University of Pittsburgh. Welcome, Tarik. Thank you very much for inviting her and is very exciting. We are able to do this research. And we're very excited to be with you here today. Nice to have you. Well, let's let's begin by reminding us what Alzheimer's does to the brain at least as far as what most researchers agree right now. What does the process look like? Both inside and out? Yes. What we know about Alzheimer's or how I would say What is the most consensual? What you know about those payments is that those primary disease is corrected. I said, mostly for the deposition of true pathological proteins in the brain. And the names of these proteins are, um, a light and Tao we know already is very well established that this deposition start moral s 20 years before the cognitive symptoms of the patient. And we know as well that this proteins are somehow associated with the narrow degeneration of the brain degeneration of the brain, and this will lead to the cognitive symptoms. This is something that established But what we still don't know is exactly how these two proteins amyloid and Tau interact with each other to determine the progression of the disease because we know This is very well established as well. We know that there are many patients or I would say more or less. 30% of the elderly, older than 65 years old have some of these proteins in the brain. But they never developed the dura degeneration in the never developed the cognitive decline associated for example, this is certainly there is a missing link. Between the deposition of these proteins in the real development of the disease. And so what Your research is showing is that this missing link turns out to be inflammation. And so how does inflammation fit into this picture of Alzheimer's now? In fact, we know that no inflammation is somehow associated, for example, this for many, many years, there are many evidence from animal models and even in humans linking the nerve inflammation for emergencies. But was never very clear how this inflammation plays out between these proteins. This deposition of amyloid and tau protein in the development of the cognition. The most accepted understanding of the disease suggest that the position of families and protein and the two main upstream events lead to the progression of the disease. What you're proposing is that no inflammation is in fact involved in the development of disease involving the first steps of the disease. What you're proposing is that individuals that have this deposition of families protein in the brain But also have the presence of information the brain Are the ones that are going to have the development on the progress of scalp pathology. That's the protein that we know that smart rose related to the symptoms and these individuals with the interaction between the amulet dogs in the brain. In the new inflammation in the brain. They were going to develop the pathology in this top pathology. We're going to cause the cognitive symptoms. So what you're saying is that we used to think inflammation was a side effect. But now we think it is the actual catalyst for this to go to to progress exactly like this. We was speaking on inflammation as a byproduct of everything that was happening, such as many others as the atrophy of the brain. But what you are saying here that no deformations, in fact involved in the beginning of the disease trigger out there the rest of the process that come in front of new information and the lighting up of dollars. So you looked at the Let's talk about how what you actually did in the study of people because it's fascinating. So you look at the living brains of people in different stages of Alzheimer's disease. What did you see? What does that progress of inflammation and tower actually look like we assess 113 videos. Any measure bring amyloid out and no inflammation. And what we saw was that the interview that havoc base length they have the presence of amyloid pathology in the brain. Any inflammation in the brain where the ones that develop dollars in the follow up and we're the ones that Developed cognitive decline developed the symptoms of dementia. We also found that individuals that have the brain only amyloid pathology that is believed to be honest. The cows of the disease did not develop the symptoms of the disease, and the ones that have only formation also did not develop the symptoms of the disease. Then our study suggests that, uh, amulet is important a market of the disease as everyone knows. But amyloid alone without the presence of no inflammation cannot lead to the progression of the towel. And consequences to the cognitive symptoms. How do you know that The inflammation is not the result of the disease and you're suggesting it's the cause of the disease. How do you What kind of data information makes you so certain about that? This is a very, very good question. As I mentioned in my last answer, I think for a bit More certain about that. We need more studies with much larger law institutional follow ups. But what gives the certainty for us was this in the longitudinal analysis? We have individuals that have the prices of information and analyze and didn't have to pathology yet. And in discharge followed that you did. They developed a pathology and this temporal association give us the inference that this would be leading to this stuff it does. I agree that much more studies are needed. And with much larger follow ups to better ascertain this this hypothesis Now is not inflammation. An immune system response. I mean, the immune system is usually coming in to protect us from something. Why would inflammation? Then why would the body go in and make Alzheimer's disease? Worse? Instead of protecting it? You are completely right. That inflammation have a lot of important and very good functions in our system. But what you believe is that when you are talking about the disease, such as Alzheimer disease, the near inflammation that's present the brain is a chronic on the reformation. And in the case of, uh, something related to our finest. This was not report to the R manuscript, and this is not studied by us but is postulated based on many students in animal models that what may be happening here. Is that the microbial cells That ourselves that are there are there as you well mentioned to protected us the microbe yourself try to clean the top pathology in the brain. The faggots site the top of dollars in the brain. And they tried to degrade this type of thought was in the brain..