Reversing Alzheimer's: New Research Improves Cognition & Protects Brain Health | Dr.Heather Sandison

I'll hear people say the cause of Alzheimer's is inflammation, the cause of Alzheimer's is beta amyloid, and that always begs the question, but why? What triggered the inflammation? What triggered the beta amyloid? And I think that's how we get to the cause. If we can ask why, why is this happening? Why did this response get triggered? Then we can get to the actual root cause, and that's where we make changes in the health of the neurons.

Well, hello everyone. I'm Dr. David Perlmutter. Welcome again to The Empowering Neurologist. I have some really amazing news for you, and that is there is treatment available that can reverse Alzheimer's disease. And yes, you heard me correctly. This is not in the form of a simple pharmaceutical intervention of taking a pill or taking an injection, but rather a much more integrative approach that pulls a lot of levers, with results that are now being published. We're going to be talking with Dr. Heather Sandison today. She's the author of the book whose title is Reversing Alzheimer's. Let me tell you a little bit more about Dr. Sandison. Dr. Heather Sandison is a distinguished naturopathic doctor and has devoted her career to providing compassionate care and innovative solutions to those affected by dementia. Renowned for her pioneering work, Dr. Sandison has integrated groundbreaking holistic and multimodal interventions, seamlessly creating clinical, residential, research, and educational platforms. Her relentless dedication has not only transformed the lives of patients and caregivers, she has also set new standards in the field of dementia care and is the author of Reversing Alzheimer's, a book that we're going to talk about today. She's the primary clinical investigator and author of the peer-reviewed article Observed Improvement in Cognition During a Personalized Lifestyle Intervention in People with Cognitive Decline, published in the very highly respected Journal of Alzheimer's Disease in August of 2023. I'm very excited about this interview, so let's get right to it. Well, hello, Dr. Sanderson. Welcome to the program.

It's a privilege to be here. Thank you for having me.

So the book is, is breathtaking. But even more so, the work is breathtaking. I mean, we live in a time— I said in the introduction about, you know, how we live in a time when there's really no straightforward pharmaceutical intervention that's at all meaningful. And we're going to double-click on that, I think, later on in the program. But you start off in the book talking about your first experience with an individual with a very low cognitive function, very low score on, in this case, the MoCA test. Maybe you can tell us what that's all about. But walk us through that vignette in your career and how, what that meant to you, what that did for you, and how it got you started.

Yeah, so I had been trained by Dr. Dale Bredesen, who you know well, and I came back from that training still skeptical. When I had first heard him present that we could reverse dementia, he had written a book called The End of Alzheimer's and was suggesting that we could reverse this irreversible disease. I had been told over and over again in my training that that wasn't possible. That to suggest otherwise was to give people false hope, it was to do harm. So to never suggest that we could help someone with Alzheimer's, that was the refrain. And I bought it, I thought that that was true. And then when I heard Dr. Bredesen explain his approach, it was this stacking of interventions, all of which I was familiar with from my naturopathic training. And the way he, the paradigm shift that he presented was that this was a complex disease, that there wasn't gonna be a single molecule intervention that was going to have an impact. And that made sense to me conceptually. And so that was why I had signed up for his training, but I still hadn't seen it work. So I came back into my office and I was now on his list of trained providers and his book had come out, it had become a New York Times bestseller, it was getting a lot of momentum and interest. And so people were showing up in my office with way more confidence than I had. So this particular patient, she came in with her husband, completely dependent on him. She could answer questions with yes or no, but no, we couldn't have a Meaningful dialogue. I could see the wheels in her brain spinning though, and she had this bright, beautiful smile and her eyes would track you. You just could see that she was there. And one of her favorite pastimes was getting dressed up. She was really into her clothing and apparel, and she was wearing this beautiful, bright floral dress and she had this studded black leather bag. And you— I could just see that she had so much personality in there, and her husband was absolutely desperate to get her back. And so I kind of went through the motions of seeing them and giving them the support I thought, you know, I was trained to provide from naturopathic school and also through Dr. Bredesen. We started balancing her nutrients. She came in with some labs already, so had a sense of what was going on. They committed to getting into ketosis. They went and got her dental work done. They were living in a moldy bedroom, and they actually moved from their bedroom into their living room to escape some of that mold exposure. They started ballroom dancing 3 times a week. And lo and behold, when she came back to See us just 6 weeks later, her MoCA score, which is the Montreal Cognitive Assessment, a way we put a number on that spectrum of cognitive decline, had risen from a 2 to a 7. So a perfect MoCA score is a 30, and a 26 and above is normal, and she was at a 2. A single-digit MoCA score is severe dementia, and this made sense. She could barely answer questions. On that, on that one-page worksheet where you identify zoo animals and you draw a clock, copy a cube, she couldn't Do the vast majority of that. Only 2 of these answers were correct. That day is one of those moments I'll never forget. I remember exactly what I was wearing and the way the light was shining in the room because it just had this— emotionally, it was so intense. I saw the difference in her MoCA score and I looked at her husband just in disbelief like, wait, what? Like, did we do it wrong last time? Like, what did we get wrong? This isn't supposed to be possible. And he assured me, he was like, no, no, she's different. And sure enough, she was. speaking in complete sentences. She was able to communicate, and they were bickering about something that had happened on their way into the visit. Their life had transformed radically. Now, she wasn't going back to work, but she was able to say, I'm hungry, I'm cold, I'm tired. She was able to communicate, and their quality of life had radically shifted. And then the next thought, after I get over the disbelief, was, Oh my gosh, if this is possible for her, what about everybody else? And how much suffering that's associated with this awful disease is avoidable? And how do we tell everyone?

Well, you know, the messaging right now, by and large, is that we have a treatment for Alzheimer's, and that is an intravenous infusion of a medicine that will target beta amyloid. And you called it out in your book. The series of medications that were the breakthrough in Alzheimer's treatment that we heard about in early 2022, and not working and fraught with risk of issues in the brain, bleeding and edema and things like that. But you even called out interestingly the the fact that there was some issues with the data that some of the images, some of the data that was presented in one of the foundational studies that made the case that Alzheimer's was the cause of Alzheimer's. Beta amyloid was the cause of Alzheimer's disease. You spoke about that in the book as well. So how do you feel these days when there is still a pretty hefty dose of advertising that we're seeing in the journals and even to the general public that here is your answer, here is the drug that's finally monumental in terms of turning Alzheimer's around? What's your take on that?

You know, it's disappointing, of course, right? I noticed that paper that you referred to, one of these very impactful, very influential papers. It's been cited, I think, over 3,000 times, 2,500 times. It's a highly cited paper. It's been used to justify the research dollars that are thrown at this beta amyloid hypothesis, and I think it's being retracted. That was recent news that I just saw. And so it's just, it's frustrating because there is so much that we can do to prevent and delay, and in some cases even reverse the symptoms of this disease. And yet so many people are still told that that's not possible and to wait on the science, it's just about to catch up, and we're just about to have this magic pill or this magic IV that's going to save us. And yet that's not how it's playing out. And so I think it's definitely sending a message, an inaccurate message of what's available right now. And so I've also been frustrated because patients who think, oh, I can get access to this medication, they go in, and if it's someone with severe dementia, they're not eligible, or if they live outside outside of the radius of a medical center where they can get the MRIs needed to track those potential side effects, they're not eligible. And the cost is extremely high as well. Yeah. I think it costs about $50,000. Some of that is covered by Medicare, but a lot of it, $8,000, not an insignificant amount, has to be covered by the patient or their family. And so, these medications, although they're first-generation drugs, right, I have hope that this isn't the final chapter of that story, right? I do hope that we'll be able to work in collaboration with the 2nd and 3rd and 4th generation medications that become available based on this kind of first go at that approach.

Well, you know, I wasn't planning to go there, but I am actually, and I'm thrilled with what you're doing. You know, I've been working with Dr. Bredesen, as you know, and a colleague for a very long time, thrilled with the notion of this multidisciplinary approach, which is the way that it has to happen. But having said that, I have a sense that these GLP-1 agonist drugs, you know, like the Ozempic-type weight loss diabetes drug that we're seeing, are going to really be quite influential in terms of how the brain is functioning and the brain's destiny. I know that there are 3 trials, 2 of which are already underway. Another one, a semaglutide trial, begins in the middle of this year. And I think they're going to show some pretty dramatic results. I mean, if it's anything like the Parkinson's results published in the New England Journal of Medicine a couple of months back, I think we're in for some big surprises as it relates to that approach. But for now, what you guys are doing is— it's kind of iconoclastic in that it uses multiple inroads, and that can be challenging for people, can't it?

Yeah, well, it's this paradigm shift, right? So we've been told that there's this single molecule, right? If you have a urinary tract infection, if you, even if you have diabetes, you can use metformin for diabetes, you can use an antibiotic for a UTI, and you can kind of resolve, if you will, for the most part, you can keep things under control, you can get rid of a UTI, it's gone, it's in the past, you never have to think about it again. With diabetes, it's a complex chronic condition, but you can take a medication and you get a solution. With Alzheimer's, we haven't had that, and I think that part of the reason is because we've relied on this outdated idea when it comes to complex chronic disease that we can find a simple intervention. And yet, it's proven again and again that we need to take a complex system science approach, that multiple pathways can lead to the same diagnosis. Memory loss in older adults can happen for a number of reasons, and they're not mutually exclusive either. You can have a traumatic brain injury and genetic predisposition and high levels of glucose and or you can have a couple of those, or you can have a myriad of others, right? So each individual, and my hope is that with AI and technology, we're gonna be better able to do this for a much lower cost, but I think that that is necessary, at least right now. And I'm in agreement with you, I think that the GLP-1 agonist will be part of that story, but we also have patients who use those, and they don't get the anticipated results. So I think that there's, it's still going to be a multifactorial story, approach that will give us the best outcomes, because there are Alzheimer's patients or dementia patients that don't have a ton of inflammation. There are Alzheimer's patients that have— they don't have metabolic disease, they have other things going on.

I think one thing that unites them all is, and I think it's going to allow us to have this kind of unanimity and understanding of all these inroads, whether it's infection, Trauma, metabolic issues, whatever it may be, that ultimately what we see in all patients is microglial activation. In other words, a change in the brain's immune system that can be induced by inflammation elsewhere in the body, can be induced by infection, it can be induced by metabolic dysfunction, by head trauma. But let me just— since I opened up infection a little bit, you talk— Quite a bit about infection. In fact, several of your graphics about all the things that lead to Alzheimer's, you include infection. And you made mention of that first patient that you dealt with, that she had mold in her home. That's an infectious agent, I guess, to some degree. But I think some of our viewers might be a little surprised with what you're about to say, that infections may tip the brain over to beginning the cascades that lead to So walk us through that.

Yeah, so we know that P. gingivalis, the bacteria responsible for gingivitis, the Lyme spirochete, as well as herpes simplex 1, these all have very well-documented relationships with the production of beta-amyloid plaque. So amyloid is antimicrobial, it's there to protect us. And when we have these infections in our system, we thought for a long time, oh, the brain is sterile, it doesn't have any bacteria that get in there. And now what we've seen in the autopsies of people who have suffered with dementia and Alzheimer's is that in that amyloid plaque, those microbes are present. And so there is this protective mechanism at play, this inflammatory response that's generated. And so, and also P. gingivalis affects the cardiovascular system, so there's kind of a double whammy because now you also can trigger inflammation in the endothelium and more of a vascular dementia picture as well as the Alzheimer's. And so, these are infections that we think about getting very aggressive about treating prophylactically, so preventing herpes simplex 1 outbreaks, in particular, really good oral hygiene, seeing a bi— I'm a fan of biological dentists, so looking for the kind of low-grade infections that we might not be associating with a toothache, but might still be irritating our inflammatory system and our immune system. And then, also the Lyme spirochetes, I think that this is an under, sort of, underexplored area when it comes to cognitive decline as we age, that when people amass these infectious burdens, right, when it's not just one, but potentially there's microbiome imbalances, there's Borrelia, the classic Lyme, but also Babesia and Bartonella and some of these other co-infections, this infectious burden creates a need for more resource, right? We need more of the nutrients if we want to get up and over that infectious burden, and so we tend to get depleted a little earlier, and that nutrient requirement goes up. It's easier to become depleted. And so I think that all of these things, right, if you have, no matter which one we're talking about, right, if you have that plus a traumatic brain injury, or plus some excessive stress, you've got cortisol that now becomes toxic to the brain, or you've got ApoE4 genetics, now all of a sudden we're stacking things on top of each other in a negative way that's going to lead to negative outcomes So

how does having had COVID-19 factor into this, as, you know, maybe from a large scale, a population level, but also for the individual?

Yeah, so you might actually know more about the research on this than I do. I see it from a clinical perspective, where I have patients come in who say, I got COVID, or even, I got the vaccine, which, you know, that's a whole nother story, but one way or another, I was exposed to COVID, and my immune system is compromised, and I'm having symptoms. My immune system responded to it, and my brain has never worked the same way since. We also have, I mean, people say the same thing after menopause, right? So there's some shift that happens after COVID for some people, not all people. And again, COVID is this amazing illustration of how you have some people who succumb to it and die, right, because of the overactive cytokine storm. Then you have other people who are asymptomatic, right? So there's this spectrum of how it impacts people. And the question is, okay, what's the terrain? Who is that individual that was affected and what were those comorbidities? What was the environment that that virus entered into so that it could take hold and create these issues? And in long-haul COVID, these long-term side effects, or these, excuse me, long-term symptoms like cognitive decline, people will say brain fog, poor energy, fatigue, debilitating at times. And so what we look for with Okay. Is there some sort of vascular piece going on? Is there some more tendency towards clotting, or is there more of a tendency towards inflammation? So we'll study the cytokines and look for RANTES in particular, although it looks like that could be protective against Alzheimer's at some level, but that's one that can become very high with a post-COVID syndrome. And so we specifically target that cytokine and look for those cytokines and then aim to get those under control.

Well, hi everyone, Dr. David Perlmutter here. We hope you're enjoying this content, and if you would do so, go ahead and hit the like button. And if you're not already a subscriber to our channel, please consider doing so. We're really grateful to have you as part of our community. So let's get right back to the presentation. You mentioned in passing a moment ago that beta amyloid being— is a form of antimicrobial peptide, or AMP. And I think that might be surprising for a lot of people to think there's an upside to this horrible protein that is the subject of all this research. To rid the brain of beta amyloid seems to be the go-to way of curing Alzheimer's, though it doesn't work. And yet you're saying that beta amyloid accumulates in the brain to help protect it against various types of pathogens like herpes simplex virus type 1, Lyme disease, chlamydia pneumoniae, Porphyria or Porphyromonas gingivalis and others. So that's kind of a different view of beta amyloid. And you made mention in the book of this kind of real lack of correlation between beta amyloid. I mean, that there are plenty of patients who have a brain load of beta amyloid to the extent that they would qualify on PET scanning of their brains for a diagnosis of Alzheimer's. That's not the only thing that would be required, of course. But yet they are cognitively normal. So there seems to be a disconnect between beta amyloid and actual Alzheimer's disease in terms of it being, you know, it's neither sufficient nor necessary to cause this disease. And you actually highlighted an upside of beta amyloid, indicating that it might accumulate in the brain in a way that's trying to help us.

I have such a reverence for the human body and the human brain, right? When we really look into these things, like, there's a reason for them, it makes sense. And I think it begs the question, I'll hear people say the reason, the cause of Alzheimer's is inflammation, the cause of Alzheimer's is beta amyloid. And that always begs the question, but why? What triggered the inflammation? What triggered the beta amyloid? And I think that's how we get to the cause, is if we can ask why, why is this happening? Why did this response get triggered? Then we can get to the actual root cause, and that's where we make changes in the health And so things like toxins, nutrient imbalances, stressors, structural issues, signaling issues, and infections, as we mentioned, all of these pieces I think can be causal. And when we address them systematically, and when we stack these interventions on top of each other, so instead of saying, oh, all of it's herpes, all of Alzheimer's is herpes, we would never suggest that, right? That would be silly. But if we say, okay, herpes might play a role, Plus, your APOE4 genetics might play a role, and the fact that you're female might play a role. We can't do anything about those, but there are all— there's this myriad of other things that we can do a ton about. In the book, I also mentioned the Lancet report, the commission report that was updated in 2020, that lists 12 modifiable risk factors when it comes to dementia and Alzheimer's. Things like obesity, hypertension, smoking, air pollution, hearing loss, treating hearing loss, staying socially connected, staying active. There is just so much that we can do to prevent and delay, and they suggest that 40% of worldwide Alzheimer's could be prevented in that Lancet article. And I think that that number is much, much higher, particularly when we add this multimodal approach.

Right, when you, as you say, stack the various modalities. Let's talk for a moment about your August 2023 Journal of Alzheimer's Disease study. a publication in which you put people through this program that is multimodal, and you had 73.9% of patients— that's a huge, you know, 3 quarters of the patients actually demonstrated in their neuropsychological testing improvement in their cognitive function. And I'm going to have you talk about that in just a moment, but I want to just present this in the context of The Alzheimer's drugs have been demonstrated to slow the rate of decline minimally. In other words, you're still falling off the cliff. You're just going to fall off the cliff in a couple of months, and you're still going to fall off and end up where, you know, at the bottom of the cliff. So there's no change in the positive direction from any of the beta amyloid-centric studies, research interventions whatsoever. You're still getting worse, but at a slightly slower rate. In the acceptance of the potential side effects of brain bleeding and brain swelling, as in 20 to 30% of individuals. Having said that, your program didn't just slow the decline, but actually led in 73.9% of the people to improvement. That's stunning. That's breathtaking. And maybe I'm shouting right now, but I feel like I should be. That's pretty incredible, pretty incredible results. Take us through what that study involved, the population, what they were pre and post, and what's next.

Thank you, and thank you so much for helping me scream about this, because I feel like it's criminal that people don't know that there are so many things we can do. So what we did was we took 23 participants. It was a feasibility trial. What we were trying to understand is, with cognitively declined individuals, will they even do this? Sometimes implementation is the hardest part of a complex intervention, and so 23 participants joined us for 6 weeks. 6 months, we did an intensive intervention with the Bredesen approach. And then what we measured was that we had a statistically significant increase in memory, overall composite cognition, both of those measured through Cambridge Brain Sciences, and then also in the MoCA scores. And those MoCA scores with the Cambridge Brain Sciences, they were 2 different ways to assess cognition, and they matched. And then we also measured quality of life and sleep, and we saw a statistically significant increase in the means across All participants in both. And then we saw increases in the means across all participants, so even the ones that didn't get better, we saw an increase in every single measure of cognition that we assessed. Now, that meant 17 of the 23, so that's the means where we saw statistical significance from the intervention. And then the question, the reason that I did this trial was because I had, I got funding, I had a philanthropist who was kind enough to ask how he could help. And the question I was getting over and over again in my office was, if I do this for my loved one, if I take the— put in the money, right, invest the time and the effort to do this for my dad or my mom or my partner, how likely is it that they'll get better? And so that's what I was looking for, was that answer that I could tell people, if your MoCA score is between 12 and 23, so remember, 30 is perfect, 26 and above is normal, so it was between 12 and 23, those are the people we recruited, all had measurable cognitive impairment. Some have a diagnosis of Alzheimer's, in fact. They were on their way there if they weren't already there. And what we showed was that 74% of the time, we could improve their cognition. Now, I think the most exciting thing about this is that I'm not the only person that's measured this, right? So Dale Bredesen, my mentor, a year before, Kat Toups and his group had also done a very similar study. They took a cohort of 25 participants, through a 9-month intervention, but their MoCA scores were only down to 19. So it was slightly less progression of the disease state, and they had a little longer intervention, 9 months instead of 6. And they saw that 84% of their participants improved. So these— my study basically corroborated their 2022 publication, very similar interventions. When people are more progressed, a shorter intervention, 74% improve versus 84%.

When people read your book, I think they're going to understand, you know, the various parts, the reducing ultra-processed foods, and most people have heard of that, the value of exercise, interaction, connecting to nature. But you talk about something called contrast oxygen therapy. So that's a little unusual for people. What does that involve?

Yeah, so I put this in the category of the hormetic effect. So hormesis is this concept that when we When we stress the system a bit, we get— of course, we're not stressing towards full decompensation, right? We're stressing so that we get more resilience. And the easiest example of this is exercise, right? When we flex our bicep and we lift, we pump iron, we, you know, we do our exercises, we're stressing the muscles so that they build strength. A fasting-mimicking diet or fasting is another example of the hormetic effect, where we're stressing the system, but we get the senolytic effect, where we get rid of those cells that aren't operating at full capacity, and we send the signals to create new ones. So we stress the system to create more resilience, which can be a definition of health, right? We also use this with hot and cold therapy. I'm sure you've interviewed many people who are proponents of, like, Wim Hof, and of getting into stressing your system to get hot, get in the sauna, right? Sauna is something that's associated with lower rates of dementia. And then getting in the cold, getting your nervous system to adapt to these stressful environments. And so, LIVO 2 is this system or this contrast oxygen therapy that where I have seen, I've had patients tell me the reason I started to use it personally and also to recommend it to some people, I would not recommend any of those things to someone frail, someone who's far down the path of dementia, I would not recommend that to. I don't want, right, we aggressively treat sleep apnea. We're not trying to get people into hypoxia when they are extremely frail or far down that path. But on more of The prevention side, where you would be doing more of the fasting and the contrast hydrotherapy or temperature therapy, where you'd be doing more significant exercise, in that state, this is something that I have seen help improve cognition for many, many, many people. So what we're doing is we're taking people back and forth from 80% oxygen down to 8% oxygen. So this isn't, it's not 0%, but it's as if you were at Mount Everest, right? It's very low oxygen. And what happens is that when you're, so you're exercising, You've got a mask on, so you might be on a bike or a treadmill or a rebounder. You want to be stationary. You're not going to take this off for a run in your neighborhood, but you're connected to a mask and then an oxygen reservoir that's concentrated oxygen at 80%. And we wouldn't want to breathe that forever. That would be toxic to our lungs. But when we go back and forth, where we breathe room air is about 20% oxygen. So just to compare, 80% is our positive oxygen and 8% is our negative oxygen. And when we Yeah. And, when we exercise with oxygen therapy, you basically can exercise longer. That's a way to do it. But, when you go into that negative O2, what you do is you increase CO2. And, my understanding of the science there is what happens when you have increased CO2 is, one, you get vasodilatory effect. It's a very, very powerful vasodilator like nitric oxide, but even more powerful. And so, you get opening of the blood vessels. You also get, as you increase CO2, you get Yeah. You get this transfer of oxygen into the cells, so you more readily uptake the oxygen that is present. And so, just like, it's not the erythropoietin type of effect, although we see these longer-term effects with the contrast oxygen therapy, we're not talking about like the athletes who are exercising at altitude and they're increasing erythropoietin and then increasing red blood cells over time. that we get in just one session. What we get in one session is a little stress on the system. So, we're inducing that senolytic effect, and we also get the blood flow basically increasing because we get these larger diameter cells. And then, when we flip to positive O2, we get this flood of good oxygenated blood that now is getting to tissues that weren't always getting it because of inflammation or whatever reason, they were not getting that capillary diffusion. as well as before. And so people have reported over and over again to me. What happened was there was a Christmas season, like, or a holiday season, December, January, where I had 3 different patients all somehow, they must have been doing some marketing or something on the EWOT, or on that circuit, because I had 3 patients end up getting this on their own. And they all told me by February, this is what made a huge difference for me and my cognition. Wow.

Well, one of the mechanisms of hyperbaric oxygen is, in fact, induction of the same element here, which is called hypoxia-inducible factor 1-alpha, which actually enhances nitric oxide. And, for our viewers, they're probably familiar with nitric oxide now. That does dilate blood vessels. It's why men take a drug to increase blood supply for erectile dysfunction based on this platform of nitric oxide. And, oddly enough, it's a feed-forward cycle. Nitric oxide actually helps to induce more of this hypoxia-inducible factor 1-alpha. And so it's, it's a misnomer because it's, uh, it's not the— it's not that it's just induced by hypoxia, low oxygen. It's induced by the change between hyperoxia, higher levels of oxygen, lower. So it's the change that it's sensitive to. It's like we used to say heat shock protein. It was named heat shock protein when people are exposed to heat. Well, it happens when you jump into cold water too, like Wim Hof talks about. So it's really, you know, it— we get locked into these names. It should be thermal shock protein, I guess. But as you, as you made very clear, you know, it's a, it's a low level of stress that's ultimately beneficial. You were talking about stressing your biceps to gain strength. But, uh, but, you know, who knows what these exact mechanisms, mechanisms are. But how cool that you're able to implement all of varied approaches with good foundation, good scientific backing, and have really just busted the notion of one drug, one intervention. And, you know, to be fair, that whole paradigm was developed as, you know, to monetize the intellectual property, right? I mean, to make that blockbuster drug. And in your book, you actually said that, I believe, that That Dale Bredesen should be given the Nobel Prize.

I certainly agree with that.

Right, and you said that, and I thought, I'm gonna second that motion. I've said that before about his work, that's for sure, but most importantly, because he's been the one who has challenged this one monotherapy paradigm where you use one drug, one intervention, and that you and he are just, you know, lighting it up now. I couldn't be more grateful. I'm grateful for so many things.

He is such a humble, kind, generous individual and obviously incredibly intelligent and an absolute genius. And he is selfless in how he has come to this work. He just is relentless. He won't stop telling people. And I just feel so grateful. He's laid the groundwork. He's paved the path so that I found my purpose in the world. I mean, my favorite thing about my work is when someone tells me, I got my mom And I would never have the opportunity to have these experiences if it weren't for the work of Dale Bredesen. So I just am— I cannot express my gratitude to him and to you as well. I mean, you also have done so much to pave the path for this work, to change the narrative around what's possible and how to think about these diseases. I mean, if you have a houseplant, I have one behind me, if it's suffering, you don't think to yourself, are there misfolded proteins? You think, does it need more water? Does it need more nutrients? Does it need more light? It's a complex organism. It's common sense, just uncommon practice that's driven by this pharmaceutical industrial complex, right? That it's gonna take patience, and there are too many desperate patients not getting solutions. They're ready to look elsewhere and find something that works.

Well, let me thank you for being with us today. Your book is wonderful, and your work is even more so. And I know that's just the beginning. I know we're going to hear a lot more from you. The August '23 article that you published in the JAD, truth be known, I was one of the reviewers of that. So I got a sneak preview of that, and it's breathtaking. I mean, for those of us who've been dealing with this issue for decades of our professional lives, We're finally seeing headway being made. And I can tell you from a personal perspective as well, watching my dad pass from Alzheimer's, you keep thinking, you know, something needs to be done. So, you know, I just am so grateful for what you're doing and getting the word out. So all the best.

So that was a surprise. Thank you for reviewing the paper. You know, that is also a selfless contribution. You don't get paid to be a reviewer. It takes a lot of time. It takes a lot of intellectual effort. And because of your review, my paper was so much better. So thank you so much for doing that and taking the time to do that.

I don't know if I did something wrong by telling you that I reviewed it because, you know, I don't know. These days nothing seems to matter though. Anyway, thanks again and I hope to see you soon.

You as well. Thank you.

Wow. What did we learn today? Cognitive decline associated with Alzheimer's disease is reversible. Now, that's pretty groundbreaking, isn't it? It's pretty landmark. And what is really unique is that it's happening without focusing on developing a single intervention like a drug, like an injection or a pill. It's a multimodal approach that has really been demonstrated, published in perhaps one of most well-respected peer-reviewed neurology journal as being effective. Again, the book Reversing Alzheimer's by Dr. Heather Sandison. It's certainly something we should all be reading, that's for sure. Thank you all for joining us today on The Empowering Neurologist. I'll be back soon. Bye for now.