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Author Dr. Dale Bredesen on Alzheimer’s Prevention

By Being Patient | September 4th, 2019

About 44 million people are living with Alzheimer’s or another form of dementia. According to Dr. Dale Bredesen, the key to preventing Alzheimer’s is to look at each person as an individual and determine what lifestyle changes or treatments for conditions that may lead to Alzheimer’s could benefit them by reducing inflammation in the brain and preventing Alzheimer’s from progressing. 

  • Alzheimer’s does not have one cause and will likely not require just one treatment 
  • Diet, lifestyle, insulin resistance or viruses like herpes-simplex 1, HIV and HHV6-A may contribute to Alzheimer’s risk 
  • Amyloid can serve as a protective mechanism in the brain, but too much may lead to Alzheimer’s 

Being Patient spoke to Bredesen about whether researchers know what’s actually causing Alzheimer’s, what future Alzheimer’s treatments may look like and how people who are worried they may develop Alzheimer’s or are in the early stages of the disease may be able to prevent Alzheimer’s or slow its progression. 

What Does The End of Alzheimer’s Mean?

Being Patient: Your book is called The End of Alzheimer’s. That’s quite a bold statement to make. What exactly do you mean when you say “the end of Alzheimer’s?”

Dr. Dale Bredesen: Let me first clarify, that is a title that came from the publisher, not from me. The book I wrote was called Wit’s End and that title reflected researchers being at our wits’ end trying to figure out what’s going on with Alzheimer’s, as well as what’s happening to your brain when you have Alzheimer’s. My wife, Dr. Aida Lasheen Bredesen came up with that title, so I thanked her and said, “I love that title, I’m going to submit that.” I also submitted ten others. They were all declined and it became The End of Alzheimer’s. Having said that, I understand why they used that title. The reality is that Alzheimer’s, which is now the third leading cause of death in the United States, as Dr. Kristine Yaffe and her team pointed out a few years ago with epidemiological studies, should be a rare disease. Unfortunately, people haven’t picked up on that yet. Prevention and early reversal are the keys and we really could make this a rare disease. This should be a past scourge, just as polio, TB and leprosy are.

Being Patient: Do researchers know what is actually causing Alzheimer’s disease since that’s being debated? 

Dr. Dale Bredesen: Some experts will tell you that we don’t know the cause of Alzheimer’s. That’s an interesting statement because it’s a singular statement: “the cause.” Who said it’s going to be one cause? And I think that this is where there’s a big and fundamental point being missed. Alzheimer’s is one of the complex, chronic illnesses. One hundred years ago, most of us died of simple illnesses like pneumococcal pneumonia and TB. Of course, the great success of twentieth century medicine was developing appropriate public health measures and appropriate antibiotics so we could effectively treat those simple diseases. However, in the twenty-first century, the vast majority of us are dying from complex chronic illnesses such as cardiovascular disease, Type 2 diabetes, Alzheimer’s disease, other neurodegenerative conditions and cancer. These are all multifactorial diseases. That’s a fundamental difference.

When people have gone after Alzheimer’s in the same way they went after pneumococcal pneumonia, looking at “one drug, one drug, one drug,” as well as “the cause, the cause,” that’s like using a checkers strategy for a chess match. It doesn’t work and we’ve proven that with billions and billions of dollars in pharmaceutical trials for Alzheimer’s drugs. It’s not the same kind of disease. It’s not that there is one cause of Alzheimer’s, at least as far as we know today. What we see is that there are dozens of contributors: insulin resistance is an important contributor, specific oral bacteria such as P.gingivalis enter the brain and they are important contributors. Specific molds and their toxins are important contributors. Specific viruses like herpes-simplex 1, HIV, HHV6-A and others are important contributors. The idea that you’re searching for the one cause is a misunderstanding.

We spent 30 years in laboratory research looking at what actually drives the process of neurodegeneration and when you look at that, what you see is many different causes. We tell people, “Imagine you have a roof with 36 holes in it.” A drug is a really good patch for one hole, but you’re now going to want to use that drug on the backbone of other things. Lifestyle is one of those, but it’s far more than that. All we are saying is something very simple: We must target what is causing the problem in each individual. It’s no surprise that it’s a little different in each person. In one person, it may be specific inflammatory processes from a leaky gut. When we evaluate this in people, we’ve never seen a single person in which there were fewer than ten contributors who had cognitive decline. We want to look early and identify all the different things. There are pathogens and we could talk about those. There are specific toxins. We can talk about those. There are specific changes in metabolism. We can talk about those. Of course, there are genetic changes. Everyone’s a little different genetically. You have to look at all these different things. So far at least, the best outcomes have been with targeting those things that are actually causing the decline.

How Should Researchers Look at Alzheimer’s Disease?

Being Patient: What do you think of the hypothesis that Alzheimer’s will be treated a lot like HIV, where it’s not just one magic pill, but many things that you’re treating at one time? Is that a good way to describe it? 

Dr. Dale Bredesen: Yes, but remember that HIV is actually quite simple. It’s just one virus. But even with that, you needed three drugs to have a big impact. Imagine HIV times ten. We’re looking at various things that actually contribute to this problem. Ultimately, Alzheimer’s disease is a protective response of your brain to numerous insults. If we’re going to treat it and prevent it most effectively, we’re going to have to determine for each person, what are the insults that it’s protecting itself from? Then we need to look at what needs to be rebuilt that we’ve lost so far. That’s the approach we’ve taken and we’ve published unprecedented improvements with that approach.

Being Patient: In your book, you mention four things that contribute to the production of amyloid in the brain. Can you describe what contributes to that production and how we can stop the dangerous part of that process to our brains? 

Dr. Dale Bredesen: In the book, we said that there are actually subtypes of Alzheimer’s. We see some people in which the predominant cause or contributor is inflammation. Then you have to find out from what? Oral bacteria, chronic viral infections and various molds or fungi may cause this. It may be from a poor American diet. All of these things are associated with chronic inflammation. You can literally trace the molecular pathways when you activate inflammation. As a simple example, one of the things that gets activated is called NF-kappa B. It’s a transcription factor and this has effects on numerous genes, including the ones that produce amyloid. You can trace the pathway from inflammation to the production of amyloid. It’s turned out as you know that amyloid is turning out to be part of the innate immune system. It’s part of your response to an insult.

Being Patient: Is it correct to think that we need amyloid to a certain extent, but we just don’t want to reach a tipping point? 

Dr. Dale Bredesen: Of course, we’ve always vilified amyloid and said, if we can just get rid of this “bad guy,” things will work. As you know, all of those trials have failed. With amyloid, it’s not that it’s good or bad — it’s both. It’s playing a role and yes, in a sense, as I said, it’s a response to an insult. You are essentially deciding, am I going to put my resources into growth and maintenance, which is what you do when you’re not being insulted, or am I going to put my resources into protection and defense? That’s of course what you’re doing when things are bad. In that sense, amyloid is a little bit like napalm. If someone’s coming across your borders and you’re trying to deal with them, you may use this, but in so doing, you are now living in a smaller country and downsizing. That’s what’s happening with this. It’s not that it’s good or bad. It’s a response.

If you find our articles and interviews helpful, please consider becoming a supporting member of our community. Frustrated by the lack of an editorially independent source of information on brain health and Alzheimer’s disease, we decided to create Being Patient. We are a team of dedicated journalists covering the latest research on Alzheimer’s, bringing you access to the experts and elevating the patient perspective on what it’s like to live with dementia.

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Dale Bredesen

Dr. Dale Bredesen

Dr. Bredesen is a professor in the Department of Molecular and Medical Pharmacology, as well as the Founding President and CEO, Professor Emeritus at the Buck Institute for Research on Aging. He received his undergraduate degree from Caltech and his medical degree from Duke.  He served as Resident and Chief Resident in Neurology at UCSF, then was postdoctoral fellow in the laboratory of Nobel laureate Prof. Stanley Prusiner.  He was a faculty member at UCLA from 1989-1994, then was recruited by the Burnham Institute to direct the Program on Aging. In 1998 he became the Founding President and CEO of the Buck Institute for Research on Aging, and Adjunct Professor at UCSF; then in 2013 he returned to UCLA as the Director of the Easton Center for Alzheimer’s Disease Research.

The Bredesen Laboratory studies basic mechanisms underlying the neurodegenerative process, and the translation of this knowledge into effective therapeutics for Alzheimer’s disease and other neurodegenerative conditions, leading to the publication of over 220 research papers. He established the ADDN (Alzheimer’s Drug Development Network) with Dr. Varghese John in 2008, leading to the identification of new classes of therapeutics for Alzheimer’s disease.  He and his group developed a new approach to the treatment of Alzheimer’s disease, and this approach led to the discovery of subtypes of Alzheimer’s disease, followed by the first description of reversal of symptoms in patients with MCI and Alzheimer’s disease, with the ReCODE (reversal of cognitive decline) protocol, published in 2014, 2016, and 2018. His book, The End of Alzheimer’s, is a New York Times Bestseller.  

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