When it comes to treating patients for cognitive decline, the traditional model has for many years been focused on the removal of beta amyloid plaques. Unfortunately, as is often the case with modern medicine, this approach focuses on treating symptoms rather than causes and is therefore only masking a larger issue. In this first episode in a series with “The End of Alzheimer’s Program” author Dr. Dale Bredesen, he and the Amens discuss how a revolutionary shift in treating patients with cognitive decline has radically changed lives.
Daniel Amen, MD:
Welcome to the Brain Warrior’s Way podcast. I’m Dr. Daniel. Amen.
Tana Amen, BSN RN:
And I’m Tana Amen. In our podcast, we provide you with the tools you need to become a warrior for the health of your brain and body.
The Brain Warrior’s Way podcast is brought to you by Amen Clinics, where we have been transforming lives for 30 years using tools like brain SPECT imaging to personalize treatment to your brain. For more information, visit amenclinics.com.
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Daniel Amen, MD: Hey, everybody. We have a very special week for you with our friend, Dr. Dale Bredesen, who’s an internationally recognized expert in dementias and the mechanism or what causes them. He’s a colleague, a friend, someone I look up to, the author of The New York Times bestselling book, The End of Alzheimer’s. He’s held faculty positions at UC San Francisco, UCLA, UC San Diego, and is the founding president and CEO of the Buck Institute.
He’s currently a professor at UCLA and has a brand new book, which is really an extension of The End of Alzheimer’s. It’s called The End of Alzheimer’s Program: The First Protocol to Enhance Cognition and Reverse Decline at Any Age. One of the big things we should talk about is Alzheimer’s doesn’t start when you’re 70. It probably starts when you’re a child. And a lot of the risk factors he talks about don’t just show up in old age. So Dale, welcome to the Brain Warrior’s Way Podcast.
Tana Amen, BSN RN: We are so excited. Thank you so much. And before we get started though, if you, to the listeners, if you learn anything, if you have questions, please post them. We would love it if you’d post it with a, like take a screenshot and post that for us. Tag us. You can also go to brainwarriorswaypodcast.com and leave us a review. We would be ever so grateful. And it will enter you into a drawing either for Daniel’s book, The End of Mental Illness, or my cookbook. But make sure you post one thing that you’ve learned because I know you’re going to learn a lot today. So welcome so much. Thank you so much, Dr. Bredesen.
Dr. Dale Bredesen: Thanks so much. It’s a real honor to be on with you two. Thank you.
Daniel Amen, MD: So the big idea is there are many roads to Alzheimer’s disease and other forms of dementia, and it really turned out to be folly looking for one drug to treat this thing that is caused by many different things. I remember hearing you lecture and you talked about the roof with 36 holes in it. How did you get this big idea?
Dr. Dale Bredesen: Yeah. And this is interesting because it goes back to your seminal paper in 2011 on CTE, where you were showing that you actually have to hit multiple things to get a result. So we, of course, we came from basic test tube research 30 years to try to understand what are the drivers, why is it that it’s been so unsuccessful to treat neurodegenerative disease?
And what we came to was that if you look at the signaling of the amyloid precursor protein, the very thing that’s giving the amyloid that we associate with Alzheimer’s disease, it becomes very clear that there are many molecular pathways that lead to this thing. And this thing actually functions as a molecular switch. When things are good, it is cleaved at one site, gives you two peptides that say, “Support brain synapses, grow forward,” you know, just like good times in a country. Same idea.
On the other hand, when things are bad, trophic factors are low, Blanco toxicity, toxins from various metals and air pollution, ongoing inflammation, all of the things that you’ve talked about before, that same molecule actually senses that. You can follow, for example, NF-kB directly to increasing genes that cause the proteins that will cleave this now at three sites, give you a completely different picture that says, “I’ve got to protect myself, I’m pulling back.”
And in fact, there’s such a great analogy. What has happened with COVID-19? We have all been told, “Pull back, social distance, stay in place, be careful, isolate,” et cetera, and so that’s been our way to protect ourselves. But what’s happened with that? We’ve entered a recession. We’re not able to have the interactions. We are literally pulling back. And that’s exactly what happens in the brain and Alzheimer’s. You’ve got an insult, you respond to it with a protection that is a protective pullback, and that’s what amyloid is doing.
Daniel Amen, MD: So let’s talk about this. We’ll get a little geeky for some of our listeners, but for many years, the amyloid hypothesis drove Alzheimer’s research. Alzheimer’s is caused by an excess deposition of this toxic protein called beta amyloid. And so there are amyloid scans, there are amyloid PET scans to look at amyloid load. And get rid of the amyloid and you’ll get rid of Alzheimer’s disease, except there has been failure after failure after failure with that model. Where do you think things went wrong?
Dr. Dale Bredesen: Yeah, and this is the problem. Amyloid is not the cause of Alzheimer’s. It is a mediator, you can say the same for [inaudible [00:06:18]. So in other words, when you have these various insults, and as you mentioned, we often tell the patients, “Imagine there’s a roof with 36 holes in it, you’ve got to patch the different holes.” As there are problems, whether they be insulin resistance or exposure to toxins or reduced trophic support, and this really is a beautiful system that you can look at very clearly how this neural network is held up, when there are problems with that, you make the amyloid as a response.
So getting rid of the amyloid is like saying, “Our company is in the red. If we just get rid of the CFO, everything will be okay. We can spend [crosstalk [00:00:06]:57].” That doesn’t help. It may give you a little extra window to spend a few more dollars, but as I’m sure you guys know yourselves, when you just get rid of the CFO, in the long run, you’re not going to do any better. And in fact, you may do worse.
And so in fact, getting rid of the amyloid, and we’ve seen a number of people, I’m sure you have as well, where when they get these anti-amyloid drugs, they actually take a dive with their decline. And then slowly, they’ll start to get a little better before the next injection, then they’ll get worse.
And one of the people this happened to years ago, I asked his wife, “So each time he got this, he clearly got worse. Why did you continue in this trial?” And she said, “That doctors know what they’re doing.” And sometimes, we don’t always, and unfortunately, in this particular case, they were doing something to this poor patient that was clearly making him much, much worse.
Tana Amen, BSN RN: And I don’t have that kind of faith.
Daniel Amen, MD: And so, let’s talk about some of the roads to Alzheimer’s. So you mentioned trophic factors, explain that to our listeners.
Dr. Dale Bredesen: Yeah, that’s a great point. So again, you can take the analogy to a country. You’ve got to have two things to make the country grow strong and building new bridges and all that. On the one hand, you have to have the support side. You have to have a strong economy. You’ve got to have a lack of inflation, major inflation, but you’ve also got to have protection from the outside. If you’ve got an invasion, people coming from other countries, that’s like inflammation in the brain. Now you’ve got a problem. That’s like pathogens.
So you’ve got to have this network. And as you know, it takes a tremendous amount of energy to keep this network up, including things like oxygenation, blood flow, et cetera. And your brain secretes these growth factors, and we kind of put these three in the same group, which are critical nutrients, things like B12 and vitamin D and things like that, and Omega-3s, things like that, and then hormones, thyroid, estrodial, progesterone, testosterone, pregnenolone, all these things, which are also supportive, and then growth factors or trophic factors.
And these are factors that, of course, Dr. Rita Levi-Montalcini discovered and won the Nobel Prize for many years ago for discovering that there are factors that bind to specific receptors in the neurons that essentially tell them things are good, support, differentiate, make connections, keep connections, things like brain-derived neurotrophic factor and nerve growth factor, NGF. These are critical. And of course, as you know, these are typically reduced in patients with Alzheimer’s.
So patients with Alzheimer’s typically have both, a loss of the overall support from these various things and an increase in the challenges in the various insults, such as pathogens from the mouth, herpes simplex, as you know, borellia from Lyme disease, molds from the sinuses. All of these have been identified in the brains of patients with Alzheimer’s. So as you indicated, trophic factors are critical for support.
Daniel Amen, MD: This is so important because many people think that with Alzheimer’s, you’re a victim of it or not.
Dr. Dale Bredesen: Right.
Daniel Amen, MD: And what The End of Alzheimer’s talks about is you can actually have some control. It’s not just a program. And I suspect your new book, the program, or how to actually do it step by step, which risk factors do you have and what are the things you can do to ameliorate them.
Tana Amen, BSN RN: So I’m assuming that also, I mean, I’m not assuming, I know because we’ve worked with you before, this is really about prevention as well and really going after these risk factors. As someone who my father was actually diagnosed, misdiagnosed with Alzheimer’s disease, so that for me is very troubling, and I know that is for a lot of people out there that you could be at all misdiagnosed with something so devastating, or that your body could even mimic, that your brain can mimic something like Alzheimer’s disease, that you could have something else. What can people do to prevent that from happening? You know, besides finding a great doctor, but what can they do to know when it’s Alzheimer’s versus when it’s like pseudo dementia and how can they prevent things like pseudo dementia?
Dr. Dale Bredesen: Yeah. You brought up an excellent point because everything, as you two know, everything in this field has been turned backwards. Everything is the opposite of the way it should be because we’ve been told that, “There’s nothing you can do. We know we don’t know the cause of this.” And so what do people say? “Don’t bother getting a genetic test because there’s nothing you can do about it.” You know, is it Alzheimer’s when you come in? They say, “Well, it doesn’t matter because you can’t do anything about it anyway. Let’s just check a few things and see if you’ve got something like your B12 is a little low.” They don’t really dive in and ask. So as you indicated, it’s important to know.
On the other hand, when people come in and they say, “Oh, we did a PET scan. It’s not Alzheimer’s. Goodbye,” well, wait a minute, you still have cognitive decline. You still need something to [crosstalk [00:12:41].
Tana Amen, BSN RN: Yes.
Dr. Dale Bredesen: Want to understand what’s causing this. And as Daniel said, these are things that the biochemistry starts much, much earlier. So even with the huge onslaught of childhood obesity and Type II diabetes and exposure to various mycotoxins, these biochemical changes can start many, many years before a diagnosis.
So for today, if there’s a question, then probably the best thing is either PET scan, and whether it’s an amyloid PET scan or an FDG PET scan. This can often pick up changes about 10 years ahead of a diagnosis of Alzheimer’s. Or spinal fluid. And of course, most of us don’t want to come in for spinal taps, but that also can indicate that there are the biochemical changes that are associated with Alzheimer’s disease.
But you bring up a good point. In the clinical studies, up to 30 or more percent of people can be misdiagnosed, or they’ll be [crosstalk [00:13:40]
Tana Amen, BSN RN: That’s crazy.
Dr. Dale Bredesen: It is crazy. And they’ll be thought to have Alzheimer’s, then they’re treated. Now, if you do have a PET scan, that drops of course.
Daniel Amen, MD: Well, we would just change that a little bit [crosstalk [00:13:51].
Dr. Dale Bredesen: Yeah, absolutely.
Daniel Amen, MD: And I do this lecture where an FDG, not an FDG PET, but an amyloid PET scan was about $3,000. [inaudible [00:14:04] go, “Alzheimer’s, yes or no?”
Dr. Dale Bredesen: Yeah [crosstalk [00:14:07].
Daniel Amen, MD: Where a SPECT scan, and there’s deep literature to support it, will go, “Alzheimer’s pattern, frontal temporal lobe, dementia, Lewy body dementia, head trauma dementia, toxic dementia, pseudo dementia, normal pressure, hydrocephalus dementia.” It’ll give you indications for all of those things. So why it’s not used as a screening tool really is based on ignorance and a lack of appropriate education.
When we come back, we’re going to talk more about, well, what’s in the program. What are specific things you can do to know if you’re headed for trouble, right? The brain is one of the few organs we don’t screen. We screen cervixes and we screen hearts and we screen breasts, but we don’t screen the most important organ, which is your brain.
Tana Amen, BSN RN: Right.
Daniel Amen, MD: And then what can you do about it? Stay with us. We’re here with Dr. Dale Bredesen. His new book is The End of Alzheimer’s Program.
Tana Amen, BSN RN: And make sure you post something you’ve learned today. I learned a lot. I’m hoping that you guys learned something. And make sure you go to the brainwarriorswaypodcast.com. Leave us a review or a question. We will enter you into a drawing for one of our books.
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