← The Neuro Experience
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- [00:00]
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If you have a single copy, and that is 25% of the population, so that is about 75 million Americans, your chance is about 30% during your lifetime of developing Alzheimer's disease. The fact of the matter is, if you start early, if you look at your blood testing, and if you then address it appropriately, Alzheimer's is truly optional.
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Above, 95% of the current cases of Alzheimer's disease are driven through lifestyle factors.
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A
So at the heart of it, what all Alzheimer's disease is.
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Now.
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B
Dale, first of all, I just want you to know that this is by far the most exciting episode that I'm probably going to do. I've been wanting to talk to you for years now. As somebody who is in the space Alzheimer's disease. I'm currently researching it. I feel like My whole life is really revolved around it because you just, I'm doing so much to understand it from a root cause and a pathological standpoint. So my first question that I want to start off with is a compelling statement that you've made and that is Alzheimer's disease is now an optional disease.
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A
Yes. And I'm so glad that you're interested in the underlying mechanisms because that is so critical to understand. And that is what has now brought us, after 30 years in the laboratory to saying that, yes, this is an optional situation now. And I know that that sounds crazy because everyone says, in fact, you can look it up. You know, Alzheimer's association, There is nothing that will prevent, delay or reverse cognitive decline of Alzheimer's. And that's simply an outdated statement. So here' why we say that it is now optional. Everyone can now get tested 35 years, 40. And we recommend you do it every five years. 35, 40, 45, 50, 55, 60, 65. And then after you get past 65, you probably want to accelerate that every couple years. No problem. It's a simple blood test. And this combines P Tau, GFAP and NFL. And we call this brain scan, which is. Because that's the most sensitive one. But there's a nice, it's a nice test done by Neurocode. They developed a highly sensitive P Tau test. And what this will do is tell you, do you have the beginnings? It's a little bit like years ago, people would say, oh, you've got diabetes. Well, then ultimately, of course, they can tell you, oh, you've got a little bit of insulin resistance. You never have to get full on diabetes. And that we take that for granted. Now, if you've got some insulin resistance, you know, maybe your fasting insulin is creeping up a little. Maybe you actually did a GTT with insulin levels. You, you can see it years ahead of time. You never need to get all the way to type 2 diabetes. Well, the same thing has happened with Alzheimer's. We can now pick this up with a simple blood test when you're relatively young. And we've got people saying, oh my gosh, you know, I'm only 45 and I've got the very beginnings. Well, please don't worry about it because we don't ever allow the dementia part to come because we now understand just what you were saying earlier, the fundamental reasons, and it's actually fascinating. So this has to do with our evolution, our evolution as a species. During our evolution, of course, evolution selected for performance over durability. And repeatedly, repeatedly, repeatedly. We have selected performance over durability, which is why we have these amazing brains you can just look at. Your ability to store information in your brain is Approximately equal to 2,500 home computers. You have an unbelievable ability, as much as the largest supercomputers in the world, to store in this relatively small, you know, 1400 gram brain, three pound thing in your skull. So unbelievable. Same thing with motor modulation, which is the thing that goes awry in Parkinson's. Same thing with motor power, where you have this unbelievable acceleration ability, which, by the way, goes awry in als. So each of these systems has been selected for performance over durability and therefore they have Achilles heels. We know the Achilles heel pretty well in Parkinson's. That's mitochondrial complex 1 in Alzheimer's. It turns out to be a number of things, but all of these fundamentally are network insufficiencies. You've got this amazing network that has a supply, dozens and dozens of things supplying it which are nutritional, sleep related, as you know, neurotrophic related, blood flow, oxygenation, mitochondrial function, ketone levels. All these things are supplying these subsystems in your neural networks. But then you've got a demand, and the demand is initially for use, but now you start coming in with the demand for protection. And you've got things like oral microbiome, where you've got the things actually, these microbes actually getting into your brain and their products, by the way, getting into your brain. You have systemic infections, you have a toxin exposure which is turning out to be one of the most common, whether it's inorganics, organics or biotoxins, things like mycotoxins. So now your supply starts to go down, your demand actually starts to go up. And what we discovered is really fascinating. You switch over from. Literally, it's a mode switch. Just as we have sleep and wakefulness. And you do different things very well with sleep versus wakefulness. You have another mode switch that goes from connection to protection. And this is what we studied when we were studying APP signaling, amyloid precursor protein signaling, you could see that there are two different modes. And the question at that time was why? Now we understand one of these is about connectivity and the other one is about protection. So when you switch over to making amyloid, you're not making the amyloid to give yourself Alzheimer's, you're making the amyloid to kill microbes. And by the way, it also binds certain metals. So it is a protective mode switch in your brain. But you are, when you're protecting yourself, you are downsizing your synaptic count. So it's very much like what happened in our country with the pandemic. We were all told, shelter in place, there's a, there's a new pathogen out there. And as we did this, of course, we went into a recession. Your brain is doing the same thing. It's pulling back to protect itself. Now when someone is evaluated, we see that early on, we can flip the mode back, we can find what's causing that and people do well for decades. And by the way, we just published a paper, it's now out, showing over a decade of sustained improvement of people with Alzheimer's, which has never been published before. So very excited about those results and the ongoing results with this. So the fact that the matter is, if you, if you start early, if you look at your blood testing and if you then address it appropriately, you, Alzheimer's is truly optional.
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- [10:29]
B
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- [10:30]
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B
20 years ago or even 10 years ago, you were, you were proposing a cognoscopy, and I believe you still are, which was more predominantly revolved around a brain scan and maybe the MOCA test. We didn't really have the option to have a P Tau217 blood test that can actually assess one of the hallmarks of Alzheimer's disease. So the fact that we have that now is, like you said, it's so simple. Just the same as if you go and get a homa IR just to assess your insulin sensitivity so it can pick up on, you know, type 2 diabetes. So this is phenomenal and groundbreaking.
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A
That's exactly right. So the cognoscopy, as you said, is blood testing, some simple online cognitive tests like CNS vital signs or a MOCA test, for example. And then if you have symptoms, you want to include an MRI with volumetrics, but if you're asymptomatic, you don't even need to include that. So it's those two, mainly those two things. Now, to the blood test where we're looking at all the reasons why you would be at risk. The P tau now adds an important dimension because it tells you, if it tells you where you stand. So the P tau is telling you, have I already begun that? Essentially it's like early insulin resistance. And then the good thing, you can actually follow it as it comes down. And we see this in our ongoing clinical trial, as people are getting better, their P tau will tend to come down. And so then you're asking, you want to know the rest of the blood test? Okay, what's driving me there? Is this about methylation issues? Is this about an ongoing infection, which is very common? People have chronic infections and don't realize it. We see it all the time. Is this about exposure to trichothecenes? Is it about exposure to mercury or to organic toxins? Is this about insulin resistance? One of the most common contributors to cognitive decline is insulin resistance. And of course, type 2 diabetes more than doubles your risk. Metabolic syndrome more than doubles your risk. As well. So common. About 80 million Americans have metabolic syndrome. So that's the most common contributor to cognitive decline. But again, if you're going to get best outcomes, you need to go in there and look at what's causing each person's decline. And often it's five or ten different things and then you've got to address those things. And what you're really doing is resetting that neural sub network back from protection to connection.
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B
Yeah. And on that, I think it would be really smart of us now just to give an underlying definition of what exactly this disease is. You know, there is so much conversation and for you and myself, you know, we understand what it is, but I think a lot of people get, they get confused. You know, what is dementia? What is Alzheimer's disease? You know, from my understanding as well, we are still looking at the definition of Alzheimer's disease as the amyloid cascade hypothesis. So let's start with what. Yeah, exactly, because you've actually mentioned so many times that amyloid is an antimicrobial peptide. And, and we'll get into that as well. But let's start with what is this disease?
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A
Yes, great point. So what, this disease, again, as I mentioned before, you've got these different sub networks, neuroplasticity network, which is what goes awry in Alzheimer's. You've got the motor modulation network. You actually use a tremendous am amount of energy to fine tune your movements. And you see that when with Parkinson's that goes awry, you can't fine tune those movements anymore. You fall down, you walk slowly, you know, your, your hands shake and then you've got the, the motor power adjust where you, of course in ALS you lose that. So if you look at your neuroplasticity throughout your brain and you look at, we look at it because we typically say, oh, people are having trouble with their learning new things, they're having trouble with memory. But it goes beyond that as ultimately they lose the ability to care for themselves. They lose the long standing memories as well as the consolidation of new information. So at the heart of it, what Alzheimer's disease is, is a network insufficiency. You've got the supply and the demand. The demand is too high, the supply is too low for numerous reasons, different for each person, by the way. So you can't just. This is why I don't like these uniform trials. We do everything the same for everybody. Well, wait a minute, not everybody has it for the same reasons. So in fact you really have like a fingerprint. You've got the specific combination of things that it with your genetics and with your exposures, et cetera. So this is a network insufficiency. And therefore you have now made that mode switch where you are switching to more. You are putting your resources toward protection rather than connection. And as long as you continue that exposure, you will downsize. Downsize, downsize to the point of death. And of course in the past nobody knew what to look for so people would just die, you know, right before us. Now we know what to look for, but you've got to keep going to find out the different things to get the best outcomes. And you're able to look at. Aha. Here's someone who had it because of a tick borne infection, Borrelia, bartonella, babesia, Ehrlichia, anaplasma. Here's another person who had it mostly because of trichothecines or ochratoxin A or gliotoxin. And here's another person who had it because of hypertension, vascular disease, things like that. So you really can look at the whole pattern of what's driving this. But as you say, fundamentally what is this disease? It is a network insufficiency that involves our neuroplasticity.
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B
Yeah. And you know what I love so much is that you talk about synaptogenesis. So we've got anywhere from around 87 billion neurons. Each neuron has what, around 5,000 connections?
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A
Yes, yes. Yeah. You end up having right around 500 trillion total synapses.
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B
Yeah. And they are the things that, the synapses which evidently come off the dendrites, they're the ones that are actually breaking down. And that's where we're seeing the network insufficiency. So you've got that. But when you talk about a supply, are you talking about mitochondrial efficiency?
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A
Yeah, great point. So what does it take for these things to be supplied? As you know, you, you, you've got about two and a half percent or so of your blood flow, basically 750 milliliters per minute blood flow going to your brain. But you're using about 20% of all your energy is going to your brain. So it is a very energetically rich, demanding region of your body. And so what happens is you are, when you're supplying it, first of all, you know, what do you have to have, You've got it's again, it's these are things are all like looking at what does it take to run a country or run a big company. Number one, you have to have the blood flow. So if you don't have enough blood flow going there, you're not going. You're going to literally have. You're going to have a smaller network that you are allowed to supply, which is why exercise has turned out to be such a critical piece. Now, the problem is everyone says, well, the most important thing for Alzheimer's is exercise. Well, yes, but that's not a cure for Alzheimer's disease. It's one thing of many that you need to optimize. So, number one, you do need to get the blood flow going. Number two, you have to have the oxygenation. I mean, you are fueling this with redox reactions, of course, through your mitochondria. So you've got to have the oxygen as the ultimate electron acceptor at the end of the chain to get the spark, to get that fuel to work for you. And so for many of us, for example, you know, you have some sleep apnea, for example, you're not going to get the appropriate amount of oxygenation. In fact, people who live at high altitude are at a slightly increased risk for cognitive decline. You don't have the same oxygenation. Of course, there are a lot of adaptive changes that occur in the body at altitude. Despite those, there is an increased risk for cognitive decline at altitude, as there is, by the way, an increased risk in macular degeneration. And by the way, we see the same thing with macular degeneration. There's a supply, there's a demand. The macula is incredibly consuming of energy, and you can literally trace the things that are driving macular degeneration. So with this, you're looking at oxygenation and blood flow, then you're looking at mitochondrial function, as you said. So you've got to have support for your mitochondria. They've got to be able to do their job. And then ultimately, you've got to have something to burn in the mitochondria. You've got the electron acceptor with the oxygen, but you've got to have a substrate to burn. And that's only two things in the brain, as you know, it's glucose or it's ketones. And here's what happens. We both, you know, we all burn glucose and ketones throughout our lives. When we get into our 40s, often now, I'm in my 70s now, so I'm an old guy, but years, 30 years ago, for me, when you get into your 40s, what's happening is you often lose both of those. You're losing the optimal ability to burn glucose because you're now developing some insulin resistance. As you know, insulin resistance can develop in your teenage years. But here's the problem. When you develop that, your insulin starts going up. As you know, when it goes up with high insulin, you cannot make ketones. Your liver will not make ketones in the presence of high amounts of insulin. So now suddenly you've lost both of the things that are required. So what we're doing and what we're doing when we get people to. You're restoring insulin sensitivity, which allows people to make their ketones as well. So at the beginning, we just start by giving some exogenous ketones because it takes a few weeks for people to be able to make their own ketones, but once they become insulin sensitive again, they can make their own ketones again. Now you have metabolic flexibility, which you go. In fact, when we were first doing this with the ketones, my wife said to me, as an integrative physician, you know, it's really about metabolic flexibility. It's not. Not just about ketones. And I was like, really? Right. So it really is. That's correct. You have to be able to burn both of those and you have to supply both of those. And so that makes a huge difference.
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B
Now, is that because, look, we. We've long known that the primary fuel source for the brain is glucose. But if we switch away from glucose and we get into a ketogenic state, and that is predominantly done through exogenous ketones or from just being in a state of ketosis.
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A
Yeah.
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B
Is that better brain energy?
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A
Not necessarily better, but for example, Stephen Kinane, the professor in Canada, took people who had mci, mild cognitive impairment. And that is, to be fair, you know, that is the third of fourth stages of Alzheimer. The four stages, Dementia is the final stage. Before that you have mci. Before that, you have sci, subjective cognitive impairment. Before that, you have an asymptomatic Alzheimer's, where. That's where P tau can help you by picking that up at that stage. So, yes, what happens is when he gave these people with MCI ketones, they clearly improved in their cognition. So it definitely helps to have some. Now, again, in the long run, as you said, you can go switch over to endogenous ketosis, but you need to be able to go back and forth. So it's not necessarily better. But here's the trick. When you are sleeping, you are naturally going into some ketosis. You don't want to eat. If you try to say, well, I'm just going to eat glucose right up until I go to bed and then as soon as I wake up, so I'll never have to worry about ketones. That has its own problems. You know, it is inflammatory, you get reactive hypoglycemia. You know, now that people are doing CGMs, what they're finding is they're waking up at 4am with glucose of 45. So what's happening? They're too much on the carb diet and so now they're producing this insulin and as they sleep now they're driving their glucose down and they're wondering, why am I waking up at 4am? That's why you're getting, you're actually going into hypoglycemia and that is not good for your brain. So the hyperglycemia is bad for your brain. The hypoglycemia is bad for the brain. What you want? This is why we like a plant rich, not plant only. It should have, you know, you could have some, some meat, some, you know, wild caught fish, some, some grass fed beef, some pastured chicken, pastured eggs, things like that. But a plant rich, mildly ketogenic diet gives you the, that smooth glucose and insulin curve. So you sleep and you do very well. And then you have periods where, yes, you'll make some ketones and then you'll come back and use the glucose and you'll go back into ketosis and these things. That's normal. And it allows you then also to have a fasting period of 12 to 16 hours at night, which is when you then go into autophagy, when you go into some ketosis and support your mitochondria that way, when you get rid of some of the trash of the damaged proteins, et cetera. By the the way, if you just prevent mitophagy, just prevent the cycling of your mitochondria, you'll develop Parkinson's.
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B
Yes.
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A
So you need fresh batteries, you need to cycle those things. So that's the sort of, again, it's a normal human way to live where you avoid cognitive decline.
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B
And you know, this obviously is going to lead me into the. You know, you've mentioned diet and I want to go into it, but this brings up the critical role of vascular dementia and protecting our blood vessels. Vessels. And of course we'll go into lipids. But before we do, I think it's also important to discuss a statistic and I want to run this by you. Do you think it's safe to say that above 95% of the current cases of Alzheimer's disease are driven through lifestyle factors and if that is the case, then can we open up the conversation of APOE 4?
- [25:54]
A
Yeah, it's a great point. Well, for sure, APOE 4 is the most important and most common genetic risk for Alzheimer's disease. And of course, you saw the paper just a few weeks ago that came out that suggested that everyone who's homozygous for APOE 4, and that's 2 million Americans, or sorry, that's 7 million Americans, about 2% of the population, it's almost 7 million Americans, that everyone will get Alzheimer's. And I think that the problem with that study is it didn't look at people who were actually doing the right thing. So if you're doing the right thing, in fact, none of those people should get Alzheimer's. Alzheimer's. So that's important. Now you say 95%. I would take a little issue with that for the following reason. A Lancet Commission study just came out saying about over 50%, just over 50% could be corrected. You know, these are things that you could avoid. But it was like obvious things like smoking, duh. We get that smoking is going to increase your chance. It's constricting your blood vessels, it's giving you more damage to your brain with the various pollutants, it's giving you more poor blood flow to your brain. I mean, on and on and on, it's all that sort of stuff. But that's, you know, that's an obvious one. So the problem is that there are many people where, yes, they may have these as an underlying, but then they also have chronic infections or so pathogens and toxin exposure. So we think in terms of the basics, we look at, you know, the basic seven things that you can do to improve your cognition and then with the specifics to you, which are, do you have specific infections, do you have specific toxin related things? And then there are things related like stress and of course, stress you can put in the lifestyle group. So I would say these combine, but I would say more like in terms of lifestyle, about 80% can be attributed. Whereas you do have people with infections and you do have people with toxins. You've got to identify those and remove those. Now, there's one caveat here which is pretty interesting. Christine Burke, a doctor who is over here in Sacramento and I call this Burke's Law, she first pointed out that if you simply do all the basics, the lifestyle things and optimize the insulin sensitivity and your sleeping and your stress levels and all that, you buy yourself 9 to 12 months of improved cognition. That gives you 9 to 12 months to look for the infections and the toxins and things like that. If you can then hit those, you will sustain your improvement and often enhance your improvement. If you don't identify them and they're there, you will. After that, nine to 12 months now, you'll start to tail off. So on the one hand, it's important for people to understand that, yes, lifestyle things are critical, but on the other hand, it's important to recognize. But by themselves, for many people, they will not be a sustainable improvement. They'll give you some period of time. So what we encourage people to do is do those basics, and then after you've done those and you've improved, start looking for. Let's make sure that you're not missing any of the various infections and toxins and things like that, because those are the ones that, when you combine them, will now give you a lifetime of good cognition.
- [29:11]
B
Yeah. Before we go into toxins, I just want to understand the risk of having one allele of ApoE4 or 2, I believe. What are we at now? Is that what percentage of the US population or global population has two genes? Because that's the one that I think people still don't understand too much about. I just had somebody yesterday who came back positive for APOE4E4. I myself am part of the average. I'm an E3, E3, kicking myself. I wish I was an E2E3, but that's okay. So let's. Let's talk about APO E4.
- [29:48]
A
Yes. So, yeah, and so I'm a 33 as well, and my wife is a 2. 3. So I said, well, I'm so envious. Do enough things right that you're not having to care for me here because she's at the lowest risk. So if you, if you are APOE4 negative, and that's 3/4 of the population, your chance of developing Alzheimer's is about 9%. It's not zero, but it's not too high. It's, you know, 1 out of 11 if you have a single copy, and that is 25% of the population, so that is about 75 million Americans. Your chance is about 30% during your lifetime of developing Alzheimer's disease. But you can drive it to virtually zero if you check these things. You get your cognoscopy, get your brain scan, do the right things. This should be something you don't have to worry about if you have two copies, and that is 7 million Americans, it's about 2%, 2.25% of the population, almost 7 million Americans, your chance is well above 50%. It depends on other genes then between 50 and 90%. But the recent paper showed that by the time you get to 80, you're up at about 88%. So their argument was, you're going to get Alzheimer's. And again, I think it's a little misleading because they're looking at just a population which is doing standard American diet and standard American lifestyle. Lifestyle. Well, yeah, that's a problem. So that really is showing us how poorly we are living these days.
- [31:22]
B
Oh, yes.
- [31:23]
A
Beyond that, you know, we also want to look to see. And so I'm dealing with a lot of people, about 10% of people of all the Alzheimer cases, 10% of them will be APOE 4.4S. And we have now an increasing number of people that will find out when they are 45. Oh my gosh, I'm a 4 4. I'm. I'm so worried, worried. Please don't worry. There's tremendous amount you can do. Let's get you on active prevention and treatment and you can do just fine. And of course, you may be familiar with Julie G. Who's the founder of Apoe4.info There are over 8,000 people on the website. It's Apoe4 positive individuals, both heterozygous and homozygous, and they share information about what everybody's doing. And they're getting some wonderful results. Results. And the vast majority of them are on some version of the protocol that we developed years ago addressing those things. Diet, exercise, sleep, stress, brain training, detox, some targeted supplements, and then looking for infections. And in fact, Julie has written about this herself. She conferred with me years ago and said, okay, things are kind of backsliding a little after she, she had had problems in her late 40s, done better, went for several years. She had basically followed Burke's Law, although she did better for more than just one year. And then she turned out to have Babesia when that was treated, boom, doing well again. And then she turned out to have some mycotoxin exposure. And when she's treated those, she's done absolutely beautifully. She's now been on this approach for over 12 years. And by the way, she started on her own own. She said, okay, I probably should be looking at these things. And before she ever contacted me. So she had already done well when she first contacted me and we started discussing. She actually wrote a part of the second book, the End of Alzheimer's Program. So she wrote the handbook part of that with my wife. So she's done beautifully.
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B
You know, it's a controversial topic, I think, because a lot of people are scared to get their genes tested. I am, on the other hand, in my honest opinion, I am advocating for everyone to do an APOE for genetic test. And you know, if it does come back and you do have some form of anxiety about this, you can get genetic counseling. But I, you know, there are some people who believe you don't have to get it. A lot of physicians as well don't think that you need to be tested for it since it's just a risk factor. Gene I'm on the end of. I think we should know, I think we should know if the bus is coming towards us so we know we can get out of the way.
- [34:00]
A
You can absolutely get out of the way. And so, you know, this is like saying, saying don't bother to get a chest X ray until you have lung cancer or don't bother to get an EKG until you've had a heart attack. I mean, it doesn't make any sense. So what's happened is because there has been nothing for physicians to offer over the years, everything is backward. They say, don't check your APOE status and that by the way, that is still the standard of care. Don't check your APOE 4 because nothing can be done about it. That that's allowing the deaths of millions of people needlessly. So yes, you're right, everyone should find out what they are. And typically you don't have to do it when you're a teenager, but you know, 35 to 40 in there. Find out your status, get on active prevention if you're positive and don't worry about it for the rest of your life. There are people who are 100 years old, documented 100 years old, APOE 4, 4, cognitively intact. So, so it can be done. And the more you start early, do the right things, the better chance you have. Then they say, oh, you gotta remove your amyloid. Well, you're. Now the amyloid invests the blood vessels as well as of course it's there to protect you. And you've got pathogens coming through the blood vessels, so it's basically slapping on there and it has an effect that's a little bit like patching a tire. So no surprise when you rip it out of there, the blood vessels bleed. And they just reported a couple of more deaths with one of the anti amyloid antibody.
- [35:33]
B
Was that Donanemab?
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A
That one was Leqembi. They just reported, that's a couple of days ago. And they reported deaths with that earlier as well.
- [35:41]
B
From brain bleeds.
- [35:43]
A
Brain bleeds, yes. And so you know what they say is, oh, we've got to learn to manage our age. No, you have to learn what Alzheimer's is all about and do the right things to treat it. I do think there's going to be a time and place for small amounts of these anti amyloid antibodies. Once you've done the right thing, you've cleaned up the inflammation, you've gotten rid of the things that the inflammation is there for, you've gotten rid of these various pathogens, you've flushed out the toxins, you're insulin sensitive, you're metabolically flexible. All things are good now. Yes. The amyloid is sitting there waiting. It's like putting your soldiers body in the A fort. They're waiting for the next attack. You can slowly move, you can take the garrison away slowly, just like you're going to move out of another country. You no longer are under the attack you were. So you don't have to leave them there. But ripping them out with these high doses and doing that as a monotherapy, it is barbaric. I mean, this is very outdated thinking that has led to this. This is something that, you know, we talked the 1990s people said, oh, maybe amyloid is causing the problem with and let's rip the amyloid out of there. That just simply has not worked. So looking at all these other things, recognizing what this disease is, which is why I mentioned you're interested in conceptually how this works, that's what leads you to the best outcomes.
- [37:09]
B
Correct? It is barbaric and it's barbaric to me that the interventions that we now know, which you've mentioned, I think at the top of it you've said quite often you bring up the numerator and the denominator. But I think if we were to look at a tree and look at right at the top, I have a feeling from everything I've read in your wonderful books and the one I'm sure that you've got coming up, you'll mention this is we have to control inflammation.
- [37:34]
A
Really. So here's the thing, because people jump on this, we've got to control inflammation. And you're exactly right. And by the way, the amyloid that we vilify in Alzheimer's is part of the inflammatory response. So it is part of your innate immune system. The evolutionarily older part of your immune system system's response to insults to these various pathogens. And it can be viruses like HSV1 or HHV6A, it can be parasites, it can be fungi. Interestingly, candida yeast has been found in the brains of some patients. It can be oral microbiome, as I mentioned. Periodontitis, things like that. Exactly.
- [38:19]
B
Periodontitis, herpes simplex.
- [38:22]
A
Exactly. Any of those things that can be. So you are now responding with this pro inflammatory response. However, if you simply damp down the inflammatory response, you have to remember it's there to help you. So what you want to do is to be able to get rid of what's causing it. That's the key. Find out, is this herpes, is this from oral microbiome changes? Is this a systemic infection? Infection, get rid of that. And you want to be able to hand over from your innate immune system to your adaptive immune system. And you know what's really interesting, Louisa, There is a parallel here between what kills people in COVID 19 and what kills people with Alzheimer's. In both of these cases, what happens is you get this massive inflammatory response and you don't have, for one reason or another, you're not handing it off to your adaptive system which clears the pathogens and then resets the innate system. So in Covid, what happens is the virus itself actually prevents you, it inhibits your interferon response so that you now don't see the virus until relatively late. And so what happens? Cytokine storm and you die of cytokine storm. Well, in Alzheimer's it's a lesser response, but you die of cytokine drizzle. So you keep. It goes along for years and years and years and you have a slightly pro inflammatory storm state for years and years and years. So what we need to do, get down that inflammation but bring up support. If you've got the right, you've got to have the right amount of zinc, the right amount of magnesium, the right amount of energetics, all of these things critical, the right vitamin D, all these things critical for your adaptive system to be clearing. Now if you're living in a house and constantly exposed to mycotoxins, it doesn't matter. You're just going to keep on, you're never going to clear everything and so you're going to keep in that state of activation. So this is why I always say, you know, great to get the inflammation down, but don't forget you've got to get rid of what's causing it.
- [40:29]
B
Yeah. You know, I live right in the heart of Manhattan in New York City. I Have it? Yeah. And it is like a. I reckon it's just a toxic soup right here. I, I walk outside and it's just my cousin is here from Australia. Australia, beautiful air quality. And he was like, Louise, because I'm struggling to breathe here. And I said really, really? And I'm so like adapted to it now. And he said I feel like I can't breathe properly.
- [40:54]
A
Did you see the report that just came out showing that people who don't smoke. So the percentage of lung cancers from non smokers is going up, up, up. And part of this is being attributed to air pollution. So if you don't smoke, great, that's a great start. But it's turning out now it's going up, up, up that you still can get lung cancer. And as I say, one main reasons turns out to be air pollution. It appears. So I think we're going to say the same thing with dementia. We already know and there are some very nice published studies showing that air pollution is associated with increased risk for cognitive decline and especially air pollution in the PM2.5 region. And especially air pollution with APOE4. So really what APOE4 does, and we studied this in the lab and published this years ago, Apoe4 is supposed to carry fish fats. Great. What the heck does that have to do with Alzheimer's? You know, it's like your butcher, it's the guy who carries the fat around.
- [41:55]
B
Wait a minute.
- [41:55]
A
It turns out it's much more interesting than that. Apoe4 binds to different receptors and is internalized into the cell. And then interestingly, about 10% of your APOE4 enters the nucleus, interacts with 1700 different gene promoters and decreases the production of things that some of them, some of which are anti inflammatory. So what happens is now you're decreasing the production. You now have a pro inflammatory state. So the net is when you are apoe4, you are more of a hyper responder to any of these things. Now that's great when you're 20 years old, but it means that as you're getting older you're now having this chronic inflammatory state. So as we know you have more vascular diseases, disease, you have much more Alzheimer's and you have a slight, you have shortevity, so you have a little less longevity. All of these things can be addressed by making sure that you don't have these things as you're going on so that you can actually do well. You look at the Chimane Indians who are, who have lots of parasites living in the third world. They do better if they are APOE4 positive. This was the primordial gene for hominids. When the hominids descended from the simians five to seven million years ago, we were all in this pro inflammatory state because what does it take to come out of the trees and walk along and you're puncturing your feet, you're eating meat filled with microbes. You've got to have this pro inflammatory response and that's what the APOE 4.4s have. But now that we understand this, there's a lot you can do about it.
- [43:39]
B
Yeah, and I want to understand as well the relationship and the difference between, you know, you've mentioned that we've got two proteins involved here. It's a multi proteinopathy. We know that there is tau and we also know that there is amyloid.
- [43:53]
A
Right.
- [43:54]
B
We've cleared the amyloid route. Right. Now we know it's an antimicrobial peptide. And that is raised. You know, the innate immune system raises it just to basically protect our brain. So we know that, but that's on the outside of the cell. Now we have to go into the microtubules and this is where we find tau. Now, I'd love to just dig into that a little bit. A little bit. Is tau also produced from the innate immune system as well, or is this due to another issue that we have there?
- [44:21]
A
Yeah, such a great point, and I'm glad you brought it up. It's, it's. And there's all sorts of studies, of course, looking at, you know, what if we now remove, hey, we removed amyloid. That didn't do much. What if we removed tau? No. And again, that's a simplistic understanding of what this disease is. So tau is a multifunctional protein. You know, in the last, it's really been now 30, 35 years, people have found that proteins don't just have one function, many of them have multiple functions. And tau is a beautiful example. It's involved in fin signaling, you know, the oncogene fin. It's involved with, as you said, microtubule stabilization. By the way, guess what? It's an antimicrobial peptide. So all of these neurons.
- [45:01]
B
Oh, Tau is as well, P Tau.
- [45:03]
A
Yes. So what happens is P. Tau antimicrobial, amyloid, antimicrobial, alpha synuclein, antimicrobial. It's like, okay, there's a pattern here. You are responding to insults, these various things, and you are downsizing. And so what happens with tau is, as you said, you've got microtubules that are stabilizing your neuronal processes. These things are sitting there just like in a house. The things that are the rafters, the beams. Beams. The tau is the bolts that stabilize those beams. So those beams. So you've got your tau that is stabilizing the microtubules. Now when you receive a signal, and by the way this relates to reelin, you may have seen there's a lot on reel and now which is another one coming in and it fits the model perfectly. So you've got these stabilization, you've now you're switching from connection to protection and you're saying, oh, I need to now pull these things back. I need to, need to be putting my resources into fighting these infections, toxins, et cetera. I've got to quickly pull those bolts off. How do you pull your bolts off? What you do is you phosphorylate the tau that changes its shape and it pops it off those microtubules. And so now you collapse those structures. So when you have a high P tau, what it's telling you is, oh, my brain is, is telling these structures start to pull back. I want to go back in the other direction. I want to lower that because I'm now putting out these processes again and making new synapses once again. So what's happening is you are recognizing you're under assault. You are fighting this. And again, P tau is an antimicrobial protein and it's a prion, by the way. Amyloid and tau are both, both prions, as is alpha synuclein. They're all prionic. Now, prions. You know, the idea was, oh my gosh, this is what's causing the disease. We're all getting infected with prions. Well, yes and no. Prions are biological signal amplification. And so if you have a single goal outcome and you don't need amplification, an example is your serum pH. You want it to be 7.5. You never say, well I want to switch to 10.4 or 2.4. Then if you get a little acidotic, you have respiratory and metabolic compensation to drive you back to 7.4. However, in other biological systems that require multi goal outcomes, literally these are switches where you're going to flip into one mode or you're going to flip into another mode, which is what happens with Alzheimer's. Then what happens is you have have positive feedback and that is prionic loops. So your prions are biological signal amplification. And a good example would be dic when you go into disseminated intravascular coagulation. You have got to make clots quickly. If you cut your finger off, if you're a cave person and you cut your finger off, you've got a clot quickly or you will die. So you switch into a mode of clotting and then you reset. Of course, if you don't reset well enough, you get pulmonary emboli and things like that. So you're going back and forth between clotting and then declotting and blood flow. And the same thing occurs with this. You're going back and forth between connection and protection. And so you're pulling back and that's what P tau is doing for you. It's fighting those microbes, it's pulling, it's popping off and it's allowing you to collapse your neurites.
- [48:39]
B
So that's primarily in the, in the axon. Axon of the cell.
- [48:46]
A
Yeah. So microtubule associated. These are in the axon. But as you probably have seen in Alzheimer's, you actually see a quote, mislocalization of tau into the dendrites. So these things are all. Again, I don't like the idea of misfolding. It's alternatively folding. It's doing its job. And the same idea with mislocalization. Well, when you say mislocalization, you're really talking about disease associated localization. But that's not mislocalization. That is responsive to insult localization. And that's the case with tau. So again, you're changing states so that you can deal with an insult.
- [49:28]
B
Yeah. The reason I asked is because we obviously know that the networks are interfered by amyloid because that sits outside of the neuron. But if we've got a microtubule breakdown and that's primarily in the axon, then I would, I was trying to think, would that then affect the myelin, which would then affect information processing speed? Maybe you get conduction block, which is similar to multiple sclerosis. And I was trying to think outside of the microtubules for a moment there.
- [49:56]
A
Yeah, no question. So this is a multi regional, multi mechanistic phenomenon. And yes, there is some axonal damage, there is some myelin damage. Not a of lot lot. It's interesting. The myelin damage is probably coming from the ongoing inflammation. So there are cytokines or damage. Interestingly, I, I work with an excellent scientist, Dr. Alexei Kurakin, who is an interactomics expert and actually developed new tools to study interactomes. And years ago he said to me, you know, if you look at the Overall signaling network. There are a lot of similarities between Ms. And Alzheimer's. I was like, whoa. I mean, we think of one as a demyelid disease and an autoimmune disease. We think of the other one as a degenerative disease. But they have both turned out to have degenerative components and to have inflammatory components. So here's the interesting thing. If you're young and you have specific pathogens, and of course the one that's emerged as the most important is Epstein Barr virus. And then you have a hyper response that is adaptive. So that's one big difference. These are people, people where it's not so much about the innate. Now they're able to trigger the autoimmune part, the immune part of it. And often what'll happen is they'll be responding against the Epstein Barr virus and they now cross react. There's a nice publication out of Stanford showing a cross reaction with extracellular matrix component that now gives you this oligodendroglial damage. It gives you myelin loss. And so that is you've got a better immune system. You got to the, you got to the adaptive part, but you now have an auto. Now what's interesting is you take 1000 people at random, 940 will have been exposed to Epstein Barr. So most of us have been exposed to Epstein Barr. One out of that 940 will develop Epstein Ms. So you can see, although Epstein Barr is crucial, it's not just about Epstein Barr. The other 939 were all exposed to Epstein Barr. None of them God ms, the one person. So it is very much about your immune system, how you're responding. And again, do you have optimal hormones and do you have optimal nutrients and all those sorts of things? So yeah, you bring up a really good point. There are some similarities, disparities between Ms. And Alzheimer's. And again, it comes back to optimizing the various players in these networks.
- [52:38]
B
Well, one thing that just stood out to me is that two out of three Alzheimer's cases are female. And we also know that the prevalence of Ms. Is greater in females. So there we, we have that in common there as well. I believe also if you're closer to the equator for ms, you've at a higher risk for, for some reason.
- [52:59]
A
But that farther from the equator.
- [53:01]
B
Oh, farther from the equator, sorry, yes.
- [53:03]
A
So you know Scandinavia and you know Minnesota, a lot of Ms. Related. And that actually has been suggested by the epidemiologists to be due to the fact that these people evolved genes that were protecting Them from zoonosis. So these people were people who had, who were, you know, shepherds and things they were dealing with, with various animals close to them on a day to day basis. And they developed genes that basically gave them a hyper response to these things. So now what happens? Unfortunately they've got the genetics for hyper responsiveness and so they hyper respond occasionally. Again, it's not everybody. It's about one out of a thousand people to things like Epstein Barr virus and that's what seems to be a associated.
- [53:52]
B
Well, just on the topic of gender now I'd love to talk about trophic support factors. And you've mentioned this as well as the, you know, we need that for. To supply, to help with the demand issue. And we're now hearing a lot about the menopausal brain. I know Dr. Lisa Moscone has, you know, she's presented a beautiful paper that came out not long ago, published a paper that shows, showed the first ever. Was it a. It was an imaging study to show that we now have estrogen receptors in the brain, in the postmenopausal brain.
- [54:26]
A
Yeah, yeah, yeah, great. It's a great point. And of course Dr. Roberta Diaz Brinton has been working on this for years. Dr. Anne Hathaway, Dr. Felice Gershon, as you mentioned, Dr. Lisa Moscone, this is a huge issue and his course, as Maria Shriver tells all of us, this is a woman centric disease, Alzheimer's. And you made a really good point. Why is it that both Ms. And Alzheimer's are female centric diseases and you know, 2 to 1 in Alzheimer's for women to men. So yes, very, very common. And you mentioned the fact that part of this involves trophic. So when we look at the major drivers of Alzheimer's disease they fall into the group of three majors and three intermediates. The three majors are energetics, as we talked about earlier, blood flow, oxygenation, ketone, all that stuff is inflammation as you mentioned and then toxicity. And the three intermediate drivers are neurotrophic activity, neurotransmitters and stress. And so when you look at the trophic support, yes, we need brain derived neurotrophic factor which we get from exercise. And you can also get it from things like whole coffee, fruit extract. And of course groups are trying to develop drugs that will increase your BDNF nerve growth factor critical for your cholinergic input. And the cholinergic input is the major early damage from Alzheimer's is in that those cholinergic nucleus in the brain and they're involved with memory. And so I break down the things that are trophic for your brain are in three groups. It's the growth factors like NGF and BDNF that we just talked about. It is hormones, estradiol. As we were studying the molecular biology of this in the laboratory, you can actually trace the molecular pathways from estradiol binding to estrogen receptor entering the nuclear altering the transcription of hundreds transcripts, hundreds of RNA species. And one of the things that does this is it increases the one that cleaves the app to put you on the synaptoblastic side on the connection side. So that so called alpha secretase increases due to estradiol's effect on the DNA. You can also trace the other side side. When you have NF kappa B, you're now increasing inflammation. It again enters the nucleus. You've got hundreds of genes affected and two of them are the ones that cut at the beta and the gamma site to give you the downsizing synaptoclastic response. So it's those two. And then the third thing is nutrients. Vitamin D, vitamin B12, these are critical for supporting your brain. But they also bring up Reelin. And so R E E L I A. There's all sorts of publication and interest in this. What they're finding is people and it's funny, they're saying okay, just like all these others, oh my gosh, we found that rein is low in the Alzheimer's brain. Let's give them Reelin. Well, why is it low? It's low for the same reason your P tau is high. Because your brain has recognized that it is shifting from connection to protection. So Reelin is all about connectivity. You're downsizing the things. Your SAPP alpha goes down, down, your A beta goes up. This is a mode switch. So this overly simplistic idea, oh, just give a bunch of reel and that'll probably help. You know, it's, it's not understanding what the disease actually is. So what happens is reelin is a protease. So it's like a molecular scissors that is involved with interacting with the extracellular matrix to allow mobility. So it's, it's a little bit like the machete. Let's say you're in a dense jungle, someone's in front of you with a machete clearing your path. That's what reelin is doing. So when you're developing, your neurons are literally migrating. But after you've finished with that, now your processes are migrating. And in both cases it takes the High reelin to allow that now, as they say. Oh, if your reelin is high and you got mistakes, amyloid, you're still in good shape. Yes, of course, because your amyloid is now sitting there in packets. It's like putting the soldiers in the fort again. You've still got the ability to go through the jungle and to make those connections. So everything's working. Yeah. You should in the long run think about, you know, decommissioning your garrisons and getting that amyloid out of there. But you're able to make memories. You still have the synaptic plasticity present because you've got that high realm. So it's telling you the signaling, your SAPP alpha is going to be high as well. You are still able to make those connections.
- [59:21]
B
And how would you essentially, I know you've written about reversing Alzheimer's and you've, you've taken people you know who have been in that state to reverse to get a mate and not being in that state anymore. How would you even go about clearing the amyloid if you've got a. Without going to lecanemab and Donanemab? How would you, can you clear the amyloid? Through therapeutic purposes?
- [59:47]
A
Yes. And it takes some time. You have to remember it's a very long acting peptide and also remember it is in multiple forms. So there's amyloid 39, 40, 42, 43. The major species are 40 and 42. And so people look at 42 to 40 ratio. The 42 is more antimicrobial, but it's also more antisocial, synaptic. That's why the 42 is more quote, toxic to your brain. It's trying to clear those microbes, but then this stuff will become polymerized. It will literally go into these big aggregates which are not very toxic. Again, it's like putting your soldiers in the fort. It's when they come out of the fort, they're fighting. That's the problem, that, that's when things are going to now start downsizing so you can clear this, this over time. Curcumin binds to it very tightly and will slowly clear it. Now it's going to take time, of course, it's going to take years. But you're slowly downsizing. While you're doing that, you make sure that you don't have a pro inflammatory state and you'll do very well because you won't have it in the more downsizing, more damaging form. Make sure that it's not, you don't have a pro Inflammatory situation in your brain. In other words, that's why make sure that all these factors are aligned. You've got your bdnf, you've got your ngf, you've got your estradiol, your testosterone, your vitamin D, your blood flow, your mitochondrial function. In other words, you're sending the signal to your network. I'm okay. I'm able to. You can go ahead and put my resources into synaptic plasticity and away from. From protection. I'm not dying from microbes coming from my mouth or the rest of my body. And you can remove it with curcumin. You can remove it. Bacopa, ashwagandha, all of these things, cat's claws, A nice one that Dr. Rudy Tanzi from Harvard showed a few years ago is another one that helps to remove this. But you know what you'll see is the same thing. The things that help to remove the amyloid are things that are anti. Anti inflammatory. Because you're saying, okay, get the inflammation down and you can begin to remove these. Turmeric, which of course is where the curcumin comes from, is very nice for this. So there are multiple ways to remove this.
- [62:11]
B
I also, I love that you brought up turmeric because I also know that it inhibits NF Kappa B.
- [62:17]
A
Exactly. It's a nice anti. Inflammatory.
- [62:19]
B
Wonderful. All right, so let's talk about some fun things. Okay? Instead of being all doom and gloom, let's talk about, you know, everyone's loving, so saunas. Is there any correlation between, I guess, amyloid clearance with this, or are we just mainly talking about blood vessel perfusion?
- [62:36]
A
Well, multiple things. A lot of it. What we're talking about is detox. And, you know, what's happened is, again, as I said, everything is backward in the. As the. In the Alzheimer's field because there was nothing that could be done. And so everybody just focused on this one thing. It's amyloid. Let's get the amyloid. And so they'll often just.
- [62:52]
B
Just.
- [62:53]
A
They'll just. They'll just, you know, intersperse one for another and they'll say, oh, yeah, oh, you know, amyloid. Oh, Alzheimer's. No, the amyloid is, you know, part of your response. And so it's not just about getting your amyloid down there. Yes, it's a nice. As Dr. Lee Hood has said, it's an important biomarker, but it's a terrible therapeutic target. So sauna. What that does is, you know, it is a wonderful part of your detox. Great study out of Finland, where people who did saunas several times a week had a much lower risk for cognitive decline than the ones who just did it once or twice a week. They didn't have it in the study because if this is a common thing to do, they didn't have people who had zero times a week. So they just looked at the ones that did it rarely versus the ones who did it commonly. Huge difference in their risk for cognitive disease decline. So, yeah, as you say so many things, it's sauna, it's, you know, filtered water, it's high, it's high soluble and insoluble fiber diets that help you to detox, all of these detoxing things. Very helpful. It's optimizing your microbiome, having some fermented vegetables and things like that. Very helpful. It's keeping your oral microbiome healthy. And you can now measure this. You can, you can look at, you know, oral DNA, that sort of thing and see if you've got a lot of pathogens in your mouth or not. That would be a concern. So, yeah, there's so. And then of course, it's playing sports, it's getting sleep. It's all the things that we realize are important, but we're now understanding the mechanisms by which they are important.
- [64:31]
B
You know, you've got, you've also got the hand eye coordination drills which you're a part of your work at Precision Brain Health over near ucla. You're, that's a component of it. I want to talk about you and everything that you're doing. I know you've got some, you've got a randomized control trial happening right now in six different sites.
- [64:52]
A
Yes. Very, very excited to be working with six absolutely outstanding physicians. Dr. Craig Tanio is down in Hollywood, Florida. Dr. Nate Bergman, who's up in Cleveland, Ohio, just outside of Cleveland in Rocky Mountain River, Dr. David Hosse, who's in Nashville, Dr. Anne Hathaway, who's right here in Marin County, California, Dr. Kat Toops, who's in the East Bay, and Dr. Christine Burke, who's just outside of Sacramento. So all fantastic integrative physicians and all getting good results with their patients. So we're in the middle a little bit more than halfway through the trial. It should be published next year, 2024. So very excited about that. And you know, the, the interim evaluation looks very positive. So we're very excited about that. So as you say, lots going on the new blood tests with ppal.
- [65:44]
B
Yeah.
- [65:44]
A
Which, which you can see at, if you go to get A brain scan. So, so now for the first time you can actually get these without paying for a doctor's visit, which is really nice. This is part of 21st century medicine to owning our own healthcare and owning our own knowledge, knowledge about this and making sure that we're doing the right things to get our best outcomes. We've trained now over 2000 physicians in 10 different countries and all over the US as you mentioned at Pacific Neuroscience Institute in Santa Monica we now have the first precision brain health program in the world which looks at this for all neurodegenerative diseases. So this is a time of real growth. I think all over the world people beginning to understand that these outdated notions that this is like, you know, a single thing like okay, everything in the brain that goes wrong is because of a misfolded protein. This is really an outdated concept. And looking at these as network insufficiencies, looking at these as we are now optimizing these networks, this has given much, much better outcomes.
- [66:48]
B
I actually might, I had did have a question based out of work from UCSF Dr. Dina Debelle who is talking about Clotho and I want what your, what your take is. Look, she's, it's remarkable. You know one of the, I think one of her trials with the gene Clotho and how it can help with Alzheimer's disease patients.
- [67:08]
A
Yeah, this is another very interesting one and I remember very well when she discovered that and first published it when she at the Gladstone and yeah, it's a, it's a very interesting genetic phenomenon and is something that is going to be interacting with the same nature network. It's less clear as you know, it's something that acts in the kidneys. It has an effect on phosphate related metabolism. It does seem to have a trophic and anti aging response. Of course it was initially shown to be an aging related gene and she was the one who actually showed that it is related to cognition as well. So it's a fascinating story and I look for more work coming out from her and from others on developing therapeutics around how do we increase Clotho.
- [68:00]
B
I think you and I need to do a part two to this. We're actually involved in the Alzheimer's awareness day together. So yeah, I just want to keep talking to you. I know that there is just so much to talk about. So we're definitely going to be doing a part two, part three and you have another book coming, coming out. I've got your book, I've got all your books on audible and I'm always Listening to them and I think they're incredible the stories that you tell. But you now got another book which is coming out on March 25 next year, which what else could you possibly write about?
- [68:32]
A
So you know, you. So that's a great point. So the idea was, you know, as we studied what happens, what is neurodegeneration about? It's always been clear over the years that neurodegeneration is somehow related to aging. You know, your chance of Alzheimer's is much higher at 80 than it is at 60, much higher at 60 than at 40. Although interestingly the area that's the region in terms of age, it's going up the most rapidly are the young people. The year over year increases in Alzheimer's diagnoses is mostly now in the 40s and 50s. It's striking. We never saw that when I was training way back in the 1980s. So understanding relationship and as you know, everything now is about anti aging. You know, now you can measure biological age, you can reduce it. We're looking in our trial are we reducing brain aging in these people? And there's this interesting and intimate relationship between brain aging and brain degeneration. They're not identical, but they are cousins, they are closely related. And so this book is about brain aging and what's the relationship between degeneration and aging and how, how all of us can make sure to keep our faculties to 100 to make sure that we can look at. So it's called ageless brain and it's looking at so many people. And I hear this all the time. We saved our money, we were going to go on trips, we were going to have a wonderful life. As soon as my partner and I, whoever that happens to be, we're going to retire at 65. But at 61, my wife or my husband or my partner develop cognitive decline. And we're never going to be able to enjoy those trips. So now, just as the it is optional about getting Alzheimer's, if you start early and look at this, the same sort of thing, you can optimize your brain aging, you can reduce your biological age as you know now. And that's been published by a number of groups like Kara Fitzgerald, for example, you can do that and there we can understand better and better about how to do that. So it's a, it's a manual for people who want to have improved brain a aging.
- [70:42]
B
Oh, I cannot wait for that to come out. We're definitely going to be able to do an in person podcast when that comes out. Dale for everyone who wants to find you. I'm going to link everything, all of your resources, everything about you below. I just want to say thank you for the work that you're doing, the public education you're putting out there, your books, and all the trials you're doing just to tell the world that this is a preventable disease, that we have a chance no matter what the genetic risk factors are. And you're really a pioneer in this space. So thank you so much for being part of the neuroexperience podcast.
- [71:13]
A
Great to talk to you, Louisa. I look forward to future discussions and thanks for all the great work you are doing.