Reversing Alzheimer's with Dr Dale Bredesen
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Welcome back to the Health Longevity Secrets show with your host, Dr. Robert Lufkin. His book titled Lies I Taught in Medical School is a New York Times bestseller. See the show notes for a link to download a free chapter. And now please enjoy this week's episode as we look at reversing Alzheimer's disease with Dr. Dale Bredesen.

What if everything you've been told about Alzheimer's disease is backwards? Dr. Dale Bredesen, author of the New York Times bestseller, The End of Alzheimer's, shatters conventional wisdom with research showing that cognitive decline can be prevented and even, in some cases, reversed. The traditional approach to Alzheimer's has failed spectacularly. Despite billions in research funding, pharmaceutical solutions have delivered really minimal benefits. Why?

Dr. Bredesen reveals the fundamental misunderstanding. Alzheimer's isn't a single-cause disease requiring a single drug, but rather a complex brain response to multiple insults. What we call Alzheimer's represents a cytokine drizzle, chronic low-grade inflammation forcing the brain to downsize its synaptic network.

Most surprisingly, amyloid, long considered the villain, is actually part of our brain's defense system. It creates little igloos around pathogens that have invaded brain tissue. This revolutionary understanding points to a completely different approach to prevention and treatment. Dr. Bredesen's protocol addresses the true underlying causes: insufficient energetic support,

excessive inflammation, and toxin exposure. His published research shows that up to 84% of patients experience improvement, with benefits sustained for over a decade in many cases. Even advanced cases show meaningful functional gains. One patient is continent while on the protocol and incontinent when he goes off it.

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Join the health longevity medical imaging revolution today. And now, please enjoy this week's episode. Hey, Dale, welcome. Robert, great to be here, as always. I'm so excited about today's topic and the importance of Alzheimer's. And I think, as you pointed out, that

You know, nobody wants to extend their lifespan or increase their longevity if they're in a nursing home with Alzheimer's or something like that. But you've had some real breakthroughs about Alzheimer's disease. And before we get into those, maybe just take a moment and

let people know what is Alzheimer's disease and then what are the things that most people get wrong about it?

Yeah, such a good point. So as you indicated, imagine that we now are improving our longevity. Everybody's looking at cellular reprogramming and looking at various things you do, reducing your epigenetic age, things like that. So imagine living to 140, but imagine spending half that 70 years in a nursing home. Is that really what you want? We want to do much better with cognition. And as I'll talk about with you today, we're

Alzheimer's is really becoming optional. We've gone from the dark ages where people say there's nothing you can do about it. We can't help you. There's a drug. It's not going to really work very well to where we can say, look, if you get evaluated, get on prevention or early treatment, you should never have to worry about it.

So the issue is dementia. And it's interesting that the Ayurvedic physicians of 3000 years ago recognized dementia and talked about it, but felt at that time that it was part of normal aging. And we now know that that's not the case. Many people make it to 100 with a very normally functioning brain.

So Alzheimer's is the most common cause of dementia. Dementia is global cognitive decline. So as people are getting a little older and, you know, we've all been told, oh, it's normal aging. You can't remember phone numbers anymore. You can't remember faces. You can't remember names and things. That's just normal. It's not. And it's really telling you that something has changed. And so what happens is what we discovered in the laboratory is

When you are having these changes, you've got about 500 trillion synapses in your brain. So you really have a remarkable supercomputer inside your skull. And then what happens is this is driven. It's got supply. It's got demand. When the supply goes down,

and or the demand goes up, things like inflammation, supply goes down from things like sleep apnea, decreased blood flow, for example, and mitochondrial function decline, or you've now got more demand, ongoing inflammatory processes, changes in your microbiome,

you know, with the sleep apnea is more on the supply side, various toxins you get exposed to, you change that equation. And so your brain is forced to downsize. And it's interesting, we all think that, oh my gosh, losing memory is horrible. Well, actually what happens is that's the canary in the mine. Your brain can function remarkably well without learning new things.

You've had decades to be pretty sharp. You know what to do. You know how to do your job. You know how to read. You know how to write. You know how to add and subtract, all these sorts of things. So your brain essentially takes the strategy, I would rather lose the acquisition of new information, which is not so critical at this point in life.

than to lose what I already have. If suddenly you woke up tomorrow and you couldn't do your job or you couldn't drive or you couldn't read or write, that would be a big impact. If you just couldn't learn new things, you could do remarkably well. And we see people do just that. So we always tell people, if you're starting to have problems with learning new things,

That's jump in, jump in early. We'd like to get everybody who's 40 years of age or older on active prevention. But if you don't do that, please, if you have these early mild symptoms, then jump in and get evaluated. Now, you know, these new blood tests are going to change the world. P tau 217.

GFAP, NFL, which is neurofilament light, and to some extent, the A-beta 42 to 40 ratio. These are going to make a big difference because we'll all be able to find out very early if we are headed for this problem. Great. We find that you can reverse cognitive decline very effectively. It gets, no surprise, it gets harder and harder as you go later and later in the course. So please do not wait.

We're now going to be finding thousands, if not millions of people ultimately who are P tau positive. In other words, they've begun those early processes of downsizing. That's really what that is telling you, but they're not yet symptomatic.

That's a good thing to know. Please don't worry about it. It's a little bit like finding your genetic predisposition that you're ApoE4 positive. Don't worry about it. There's a lot you can do about it. And as you indicated, yes, we've published trials and various cases of people who have reversed their decline very effectively. And by the way, we have a paper in press now showing people who have reversed and sustained their improvement for over a decade.

Yeah, I definitely want to talk about those. But just to emphasize one thing that you said, I want to make sure everybody heard that, is that is...

that while gray hair and wrinkles may be an acceptable normal sign of aging, cognitive decline is not. And so if people are experiencing cognitive decline, it is a canary in the coal mine. It's a red flag. They need to pay attention to it. Now,

Alzheimer's disease, I think you may have pointed this out in one of your books, but it represents the ultimate failure of the medical research establishment in that we had literally decades of time and almost infinite financial resources being thrown at this disease. So why...

How come everybody's gone off the rails? And what have you been, how were you able to, what did they miss there? It's a great point. And, you know, we're all trained, as you know, when we are trained as physicians, and this goes back to your book, I think very nicely, we're taught things that turn out to be incorrect. And

And so when people looked at what can we do about Alzheimer's, they started with some assumptions that turned out to be completely wrong. So they said, we want to find a single drug that cures this process. Well, it's not a single drug process. It's a complex process.

brain synaptic process that is changing. And so presupposing that you would do this is, it turned out to be wrong. Second thing, they said, we'd like to find one drug that's for all patients. Well, patients get Alzheimer's for different reasons.

Some people, it's more about ongoing inflammation. Some people, it's more about reduced blood flow. Some people, it's especially about their sleep apnea. Some people, it's about changes in their oral microbiome or gut leakiness and on and on. There are many processes and you can boil them down basically to those three buckets of

Too little energetics, too little support, basically. Too much inflammation, putting drag on that system, or too much exposure to various toxins. And those can be things like air pollution, as you know. They can be things like mercury amalgams. They can be things like organics, glyphosate and toluene and benzene and formaldehyde. Or they can be things like biotoxins.

Things like trichothecines and ocrotoxin A and gliotoxin and things like that. So the reality is we are exposed to these various things. What we call Alzheimer's disease has turned out to be the brain's response to these various insults.

So it's just like when you're putting out, for example, cytokines. So there's actually some analogy here with COVID-19. When you get assaulted by a virus, you have cytokine responses. You now have T-cell responses and B-cell responses. You have the whole adaptive thing. But the problem and what kills people, as you know,

with COVID-19 is cytokine storm, this pushing out from the innate immune system. With Alzheimer's disease, you're not dying in a few weeks of cytokine storm. You're dying in a few decades of cytokine drizzle.

So what's happening is you're getting a little bit of this ongoing innate system activation, ongoing inflammation. And that can be from tick-borne illnesses or various other infections, whatever causes that. It can be from a poor diet. All of these things can contribute to this ongoing inflammation, which ultimately is causing you to require to downsize your synaptic network.

And so I think people got it wrong because they wanted a single drug. They wanted it to be the same size for all and

And they wanted to have it be simple, like, okay, it's just gonna be one thing. The biggest problem is people don't agree on what the disease is. So there are people who believe that this is nothing more but amyloid production. And amyloid is actually a part of your innate immune system. It is your protection against these insults. So sure, as with other cytokines, it can damage your brain, it can damage cells.

But it's there not to give you Alzheimer's. It's there to deal with these various pathogens and things like that. So I think that people had it backward. And so because of this, they say, well, there's nothing we can do. So don't come in early, which is the opposite of what it should be. Don't check your ApoE status, the opposite of what it should be, because there's nothing you can do about it.

take a drug that has virtually no effect and all sorts of horrible side effects and just be satisfied with that. So that is all backward. What we find is that you can be absolutely proactive,

For everyone who, as they turn 40 or they're already older than 40, please get a cognoscopy. Just as everyone knows, we all know when you turn 50, what do you get? You get a colonoscopy. So if you're 40 or over, please get a cognoscopy. It's pretty easy to do. You can go online, MyCognoscopy. It's a series of blood tests that is looking at these parameters. Do you have inflammation? Do you have a reduction in trophic support for your brain? Is your vascular status poor, etc.?

It is then a simple online cognitive assessment. So we're looking at where do you stand? It takes about 20, 25 minutes or so. And then thirdly, if you're already having some symptoms or if you're scoring poorly, of course, you want to include an MRI with volumetrics. And obviously, you're an expert in this area. So that really helps to tell you, is your hippocampus

shrunk? Is it atrophied already? And so these things are all helpful to know. Then you can get on an optimal program. If you've got inflammation, you want to deal with that. You want to determine what caused it. So you really want to get to the bottom of this. And we've trained over 2,000 physicians in 10 different countries and all over the U.S. who are very good at doing this and making sure that people get on the right things. When they do that, the outcomes have been unprecedented.

Yeah. And just to shout out for your first book, The End of Alzheimer's, and all the several books since then, but I highly recommend it. It's very readable. It's a great overview of this whole process and all these subtleties you really explain in detail. But there's sort of a misconception out there that Alzheimer's is a one-way street. In other words, you get it and you go downhill and it's game over. There's nothing you can do. And

Well, actually, as far as accepted pharmaceutical prescriptions, there are none that really work from our mainline system. But you've shown in your prospective controlled studies that this isn't really true, and you've gotten some dramatic results. Maybe you could share those with us.

Absolutely. So the idea here is once you realize what this actually is, it's not just about amyloid or tau or prions or free radicals or herpes or, you know, on and on and on. The type three diabetes is another thing that's used. And that's certainly a part of it. But once you realize that the fundamental nature of what we call Alzheimer's is a network insufficiency. So

Imagine you have a very complicated country. I mean, you know, the brain is complicated. Imagine you have that. And now you're looking at, OK, there's a little bit too much on the people coming across the borders. We got to deal with that. There's not enough coming into the coffers. We got to deal with that. OK, you've got to have multiple places where you hit this. And so what we do then is we evaluate people to determine all these different things and

And then we address the ones that are abnormal. We improve their support. We improve their blood flow. And by the way, one of the things that's worked very well as a part of the overall program is called EWOT, Exercise With Oxygen Therapy. It improves blood flow and it improves oxygenation.

We also want to make sure that sleep apnea is not a problem and dropping your oxygenation status at night, which for so many people, that's a contributor. And then, of course, there's a lot of information now showing that specific organisms from your oral cavity get into your brain. So you have things like P. gingivalis and T. denticola and F. nucleotide and prevotella intermedia, all these things.

actually have access to your brain. Of course, you know, you and I were taught in medical school

that the brain is a sterile organ, you never get stuff in there. Well, it turns out that that's what the amyloid is doing. It is surrounding, like little igloos, it is surrounding these organisms and killing them. So when you see a lot of amyloid, it's not there to try to give you Alzheimer's. It's there because your brain had these insults from these various pathogens, and it was responding by getting rid of these pathogens.

So we can think of the program in two ways. There's the basics and then there's specifics. So the basics, there are seven.

Diet, exercise, sleep, stress, brain training, detox, and some targeted supplements. You know, it works best to get people on a plant-rich, mildly ketogenic diet. That's improving their energetics. And in fact, people can even take some ketones at the first couple of months and they see improvement. This was shown by Professor Stephen Kinane in Canada a number of years ago. People with MCI actually improved just by taking ketones.

because you're now giving the brain a support that it did not have before. When we see people with cognitive decline, they've lost the ability usually both to utilize glucose and ketones. Your brain can only utilize those two things.

Glucose, ketones. They lose both as you become insulin resistant. Your insulin now goes up. Your brain doesn't use glucose very well. And now because of the high insulin, you can't make ketones. So as you know very well from studies of PET scans, that's the hallmark of Alzheimer's disease, reduced glucose utilization in the temporal and parietal regions, and especially in

Areas like the posterior cingulate and the precuneus and things like that. But that's the hallmark. It's showing you that there's a problem with metabolism here. And so when we treat these people, we do those basics. And then we look for the specifics, which are, do you have specific infections that have been missed?

And I have to say, Robert, I have been so surprised. People will say, well, you know, I don't have any infections. I'm fine. And they'll turn out to have chronic babesiosis, chronic Bartonella, chronic Borrelia. We had one recently, a woman who did well for six years, perfect, went up from 24 to a perfect 30 on her mocha, six years, started to go downhill.

And so, okay, what's been missed? What's going on? Something new? She had three things. She had a new sinusitis from Cryptococcus laurentii.

It's an uncommon organism. I don't know where she picked that up. The second thing she had was sleep apnea that had not been diagnosed earlier. Probably it had gotten worse. And she had severe AHI greater than 40. And the third thing she had was they had a new leak in their roof, which actually had brought water into the house. They had some damage and some mold growth. And she had mycotoxins that were shown in her urinary sample.

Those three things were treated right back up, doing great again. So, you know, we've always seen as physicians and we've been taught, you know, as neurologists,

Alzheimer's, we don't know what causes it. There's nothing to do about it. You're going to die. Take a trip around the world, these sorts of things. That is all outdated now. Basically, this should be a rare condition. We can determine what's driving it. We can do something about it. We can prevent it. We can reverse it in many cases, not all. And as you get farther and farther, it's more and more difficult. And having said that, we have people with MOCA scores of zero,

who are, you know, aphasic, incontinent, cannot take care of themselves, who've come up at least to fours or fives, that's not a lot, but they can speak again. They can engage again. They're continent again. One of the patients literally goes, when he's on the protocol, he's

continent. And when he's off the protocol, he's in continent. You can just go back and forth. So there is so much more that we understand about this problem. And definitely, if you're going to live to 100 or 110 or 20 or 40 or what have you, you want to do it with a functioning nervous system. Well, I have to ask then if...

I mean, with these kind of results out there, what is the pushback from everybody? Why isn't everyone doing this? I mean, you could cynically say with type 2 diabetes, well, there's vested interests in dialysis and amputations and selling insulin. But who makes money off Alzheimer's disease? Why isn't this message getting out there more, Dale? What's going on?

You know, that's such a good point and I appreciate your asking it. So I would recommend everyone take a look at two nice documentaries.

And one of them, I have to say, beaten my own chest. One of them is about this work, but the other one's about MS. And I just actually saw this and I was really impressed by it. The MS one is called Living Proof. It's on Amazon. And it's about a guy who is basically trying to do the same sorts of things with MS treatment and is getting all sorts of pushback from the MS foundation. You know, you can't do this. And, you know, we got to push the drugs and all this really sad stuff.

And the other one is called Memories for Life, Reversing Alzheimer's. And it's narrated by Michael Buble, who did a great job. And it's about this work that we've been talking about today. And it's also on Amazon. And it really shows they have some discussions with the Alzheimer's Association. And the bottom line is just exactly what you'd imagine. Follow the money.

When you're talking about a drug for Alzheimer's, you're talking about a hundred billion, with a B, dollar drug,

So the pushback is not surprising. I understand that that's the job when you're trying to make more for your investors. Of course, you're going to focus people on that approach, despite the fact that it has not led to improvement, let alone sustained improvement in people with Alzheimer's disease. I do think in the long run, drugs will be very important for Alzheimer's,

combining them with these optimized precision, what we call precision medicine protocols, where you're looking at what actually causes, you know, and are we surprised that it's what actually causes the disease that's the right thing to target? You know, that makes a lot of sense.

And as you know, and you've written about, you know, these are functional medicine sorts of approaches. So my argument is precision medicine protocols combined with targeted drugs. That's the way of the future. And I think that's that's what's coming. But as long as you've got people who are looking at making hundreds of billions of dollars for

from denying the publications, of course, that's what's gonna happen. Now, to be fair to the naysayers, what they've always said is we want more data. Okay, so we published 10 cases and we published another 10. We published 100 cases of documented improvement. That was 2018.

We published then a proof of concept trial that was 2022. Then in 2023, Dr. Heather Sandison, one of the colleagues and one of the ones who took our training early on, published her own confirmatory trial. They did very similar things. They've had very similar results. People improved in most cases. Now we're in the middle of a randomized controlled trial. So everything to date has worked.

And the pushback is, but we don't believe it yet. We want more and more. And so, you know, the bar keeps being raised, where on the pharmaceuticals, the bar keeps being lowered. It didn't work for dementia. So then they moved to MCI, mild cognitive impairment. And they're saying, well, you know, it doesn't really make you better, but it does seem to slow the decline a little bit. Now, to be fair, anti-amyloid antibodies are

Bapineuzumab failed, Solazumab failed, Gansanarumab failed, Cronazumab failed. All these things failed. Aducanumab failed in one trial, succeeded in another trial, minimal impact. Whereas Lucanumab, it did look like it slowed the decline in early, the MCI in early dementia patients by 27%.

But as they say, 27% slowing is not clinically significant. It's statistically significant. It's not clinically significant. You can't tell the difference between people who went on it and didn't go on it. It's a half a point on an 18 or 16 point scale, I guess, 16 or 18 point scale. I forget which it is, but that sort of teens scale, a half of one point. That's the difference.

So we can do far, far better. And I think that that's with these new blood tests and with some of the aging interventions that people are doing where you're changing epigenetics of aging. These are going to come together and really make it so that people see, oh, yes, there is something we can do about Alzheimer's. And in fact, we can do it. And it's just going to get better and better over time. So we're in that phase.

really interesting period where there are all these deniers, just as you said. How come people won't get this? We've had such strange things where we'll send in you an op-ed. People should be aware of this. We do this. No, they won't publish the op-ed because they are supported by the drug companies. We had one time when we published our trial that was clearly successful, 84% of the people improved.

we actually went to a group that does internet PR to get this out. And they said, no, we can't put this out because we are paid a lot by Biogen, the drug company, and anything that could get in their way is going to make it so we lose that contract. Well, okay, how do you get the information out other than just show the data? So it really has been surprising to me. I've learned a lot about how

how powerful the structure, the infrastructure of money-making actually is. And okay, I get it. You're trying to make money for your investors. But to the point of watching people die, that's been really sad for me to see, that you'd rather push on these things that are letting people go downhill needlessly than

than to just say, well, you know, there is something here. You might want to consider trying. Here's something that's been peer-reviewed and published. So, you know, I see this as at some point this is going to be the next opioid scandal where people are just pushing things inappropriately and suppressing things inappropriately. And so I look forward to the day when we can all work together to say, hey, let's combine these things. Let's get even better outcomes.

Yeah, hopefully sooner rather than later. I want to, before we run out of time, I want to emphasize one thing you mentioned before is that Alzheimer's disease, it's not like an on and off switch that you suddenly walk in and you get it once. And even by the time your doctor diagnoses the MCI or mild cognitive impairment, or you notice it, or even then, chronologically,

the disease has been going on for years, if not decades before that. So isn't it really in our own best interest to be vigilant for any of the signs and

Also, even the tests, you know, the APOE4 allele that you mentioned, it's also a risk factor for inflammation in the heart and other diseases. And a lot of the things that, you know, cause Alzheimer's is multifactorial, certainly, but, you know, insulin resistance for the, you know, the diabetic ones or the, you know, the toxins that we may have in our environment, the mold that may manifest as Alzheimer's, it may manifest as something else beforehand. So it's kind of

All of the lifestyle, toxin, functional medicine, things that we can look at in our lives, even if we're not diagnosed with diabetes or Alzheimer's or heart disease, we should be vigilant about them because all of these diseases are in progress at some point. And if we're going to live a long life, which increasingly longevity is increasing for all of us, that we need to pay even more attention on these. Yeah.

So glad you brought that up. I think this is one of the most important things to recognize because actually it gives us an advantage. We can see these things coming. So as you know, way back in the 1940s and 50s, either you had diabetes or you didn't. Then people started realizing, well, wait a minute, before you ever get there, you have a period that can be fairly long of pre-diabetes. And then they started realizing, well, wait a minute, before you get to pre-diabetes, you have a period of insulin resistance.

Wow, this is great. So now we can all check to see, even in our 20s and 30s, are we already getting insulin resistance? Addressing that can prevent you from ending up with all these terrible complications of type 2 diabetes. So we should all know that. Well, the exact same thing is happening now with Alzheimer's.

Before you get dementia, you have mild cognitive impairment. And I still remember the late Leon Thal, professor at UC San Diego, telling me when I the first time I ever heard the term mild cognitive impairment. This was in the 90s and saying, you know, before you get there, you have this thing. OK, well, before there you get to MCI, you have SCI, subjective cognitive impairment.

And before you have that, it's very clear you have an asymptomatic period that can last several years where you can already pick up these things. This is why these blood tests are going to change things so dramatically. So we should all know the most important test we can get this year, and I've actually just set up to get it, is to look at your phosphatidyl. We've been calling this brain spam. It's three tests, P-tau-217,

GFAP and NFL neurofilament light, most important tests you can get this year. It will tell you if you're in that early period, are you headed for this? You don't have to worry about it. Don't say, oh my gosh, I'm headed for Alzheimer's. You know, I'm really depressed. No need. It's like saying I have early insulin resistance and I'm going to prevent myself now from getting diabetes. Great. Now we can all, this is why I say this disease is becoming optional.

we can all prevent ourselves from having Alzheimer-related dementia by finding out early that things are headed. It doesn't mean you have it. It means that they're headed in that direction. Now, it's interesting. The pharma group and people that they pay, paid consultants, just had a big meeting to say, well, let's get this test for everyone and put everybody who's abnormal on the drug.

Which is the opposite of what you should do. Yes, I completely agree we should all get the test. But the whole point of getting the test is to avoid the drug, not to sell more drugs, is to do the right things so that you never progress to the point that you need treatment for Alzheimer's related dementia.

We should be able to reduce the global burden of dementia and therefore keep people sharp as long as they want to live. 100 years, 120 years, whatever you're going to live, you're going to have to keep that network supported and not too much inflammation, toxicity and stuff like that. We can do that now. And having these new measurements is an important part of that. That's such a great, great test. Is that covered by insurance? Or if not, what is the cost of it?

That's a great point. And it is not yet covered by insurance. I hope that will be coming. So no surprise, some of these first tests came out, they said, well, now you don't have to have a PET scan. So we're going to charge you over $1,000. We've actually been working with one of the groups to get the price down, down, down, down. And so it looks like we're going to be able to get all three of these tests covered.

for somewhere in the 500 something. Now it's still expensive, it's 500 something dollars, but it's not a $5,000 PET scan. It's not even a $1,300 scan from other companies. It's much better. And it's such a critical piece. Just as we all know our blood pressure, our cholesterol, we should absolutely know our P-tau 217.

Great, great point. Well, well, Dale, how, how can people find out where you're getting in touch with you on social media and also get in touch with you if they have Alzheimer's patients and where you're practicing now, what's the best way for them to get ahold of you.

Yeah, thanks so much. So you can do it through Facebook, Dr. Dale Bredesen. Same for what used to be called Twitter, now called X. Also on Instagram, same thing. We're setting up the first precision medicine program for neurodegenerative diseases of all types at the Pacific Neuroscience Institute. Very excited to be working with Dr. Dan Kelly and Dr. David Merrill.

on that. So that, I mean, my hope is that we'll be able to offer hope to people from all over the world who have various neurodegenerative conditions. And so I think all of those are good. And then you mentioned the book earlier, The End of Alzheimer's. We have another one called The End of Alzheimer's Program and a third one, which is called The First Survivors of Alzheimer's. So all of those places are good places for information.

Well, this has been a great conversation. Thanks so much for spending time with us, Dale. And thanks so much for all the good work you do. I look forward to grabbing that cup of coffee with you in Santa Monica, too. I do as well, Robert. Thanks so much. If you're enjoying this program, please hit that subscribe button or even better, leave a review. Your support makes it possible for us to create the quality programming that we're continually striving for.

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