Tarek Pasch, Tarik, 113 Videos discussed on Science Friday

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Friday. I'm Ira Plato. The brain of a person without timer's disease has a few Hallmark traits. First, there's a build up of plaques of proteins called amyloid Beta. Second are 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's 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's 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 that process look like, both inside and out? Yeah. What do we know about Alzheimer's or how I would say What is the most consensual? What you know about those Hammers is that those image disease is characterized mostly for the deposition of true pathological proteins in the brain. And the names of these proteins are amulet and towel. We know already is very well established that this deposition start more or less 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 that their generation of the rain and this will lead to the cognitive symptoms. This is something that established but what we still don't know is exactly how this true proteins amyloid and Tau interact with each other to determine the progression of the disease. Because we know this is very established as well. We know that there are many patients or I would say more or less. 30% of the elderly's older than 65 years old have some of these proteins in the brain. But they never developed their audition aeration in the never developed the cognitive decline associated Four languages. Certainly there is a missing link. Between the deposition of these proteins and 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 inflammations fit into this picture of Alzheimer's now? In fact, we know that information is somehow associated for Simon this for many, many years. There are many evidence from animal models and even humans linking the negative formation. If I was like this is But was never very care. How does information plays out between this 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 family protein and the two main upstream events lead to the progression of the disease. What you're proposing is that no information is in fact involved in the development of the disease. Involving the first step. Just the disease. What you're proposing is that individuals that have this deposition of family 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 pathology. That's the protein that we know that smart clothes related to the symptoms and this interview 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 type of 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 progress exactly like this. We was to figure out 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 information is in fact, involving the beginning of the disease in the trigger out there the rest of the process that come in front of nerve formation. I'm delighted. 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 looked at the living brains of people in different stages of Alzheimer's disease. What did you see? What does that progress of inflammation and to actually look like? Yes, 113 videos. And we measure bring amyloid out and notice formation. And what we saw was that the interview that have a baseline they have the presence of amyloid pathology in the brain. Inflammation in the brain, where the ones that develop pathology in the follow up and where the ones that Developed cognitive decline developed symptoms of dementia. We also found that individuals that have the brain only amyloid pathology that is believed to be on 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 market of the disease as everyone knows. But amyloid alone without the presence of the Reformation 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 institutional follow ups. But what gives the certainty for us was this in the longitudinal an artist. We have individuals that have the prices of inflammation and, um like and didn't have to pathology yet. And in this charge follow up that you did. They developed a pathology and this a temporary association give us the inference that this would be leading to this stuff at all. I agree that much more studies are needed. And with much larger follow ups. To better a certain 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 a disease such as Alzheimer disease, the nearest summation that's presently brings a chronicle near information. And in the case of, uh, something related to our findings. This was not reported the R manuscript and this is not studied by us, but it's supposed to lated 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 protect us. The microbial cells try to clean the top pathology in the brain, the faggots site to pathology in the brain. And they tried to degrade this type of knowledge in the brain. When they degrade the stuff pathology, the brain. There are something called house It's in this. Thousands are a part of the top protein that escaped generate Marta. And along the way he will be released this house it's and this thousands generate new town. For this reason, the note inflammation that's there, probably in relation to the amyloid pathology that attracted the great town is in fact propagated in the brain. So the brain has good intentions. But it's going down the road to hell. Is actually they. My problem has good intentions..

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