Dale bredesen has collaborated on the publication of more than academic research
Dale bredesen. Bredesen received his undergraduate degree from the California Institute of Technology and his medical degree from Duke University.
In Dale bredesen episode, Dr.
Although the subtypes vary in their and manifestation and often overlap to some degree, Dr. Bredesen explains that the underlying pathological features — the accumulation of amyloid beta plaques and tau tangles — are unifying aspects of the disease. He adds that how these features
Dale bredesen out in the somewhat fragile environment of the brain depends on a wide array of parameters, such as genetics and lifestyle factors, including diet, sleep, exercise, and environmental exposures.
Click here to read Dr. It is a known neurotoxin that destroys nerve synapses and then clumps into plaques that lead Dale bredesen nerve cell death. But in recent decades research has revealed interesting
Dale bredesen that suggest amyloid-beta can play a protective
Dale bredesen against fungal, bacterial, and viral infections.
One example is seen in the herpes virus, which upregulates Dale bredesen production of amyloid-beta protein in vitro. In turn, the binds to and agglutinates the viral particles.
There may be good reason for this antimicrobial property too: Animal Dale bredesen demonstrate that chelating agents can even reduce deposition of amyloid-beta. These interactions with metals become important in the discussion of Dr. Click here Dale bredesen a FoundMyFitness episode featuring guest Dr. Gordon Lithgow discussing metals in the context of aging, protein aggregation, and neurodegenerative disease.
A key element in the acquisition of knowledge about our risks factors and what can be done to manage our risks is what
Dale bredesen. Dale bredesen proposes a pretty radical idea: The key to doing this? However, a recurring theme a recurring theme throughout our discussion with Dr.
Bredesen is that what most labs and clinicians call normal may actually be different than what is optimal.
Whether a person is at risk of developing the disease versus actively manifesting symptoms is Dale bredesen reflective of the number of their suboptimal biomarkers: View a more Dale bredesen list at popular APOE4 community site apoe4. I'm really
Dale bredesen to be sitting here with Dr. Dale Bredesen, who is internationally for his understanding of the mechanisms of neurodegenerative disease, particularly Alzheimer's disease.
In fact, he was the founding president and CEO of the Buck Institute back inso that's really kind of cool. And he also is an author of a "New York Times" best-selling book called "The End of Alzheimer's Disease," bredesen I'm sure we're going to quite a bit about today. It's got a really interesting multi-pronged protocol for preventing also helping treat mild cognitive dementia and Alzheimer's disease.
So thank you so much, Dale, for having me here at your place. So maybe we Dale bredesen start a little bit by just talking about some of the characteristics and pathological distinguishing features of Alzheimer's disease and maybe what your thoughts are Dale bredesen what can cause Alzheimer's disease or leads to it.
Right, so it's a good point because cognitive decline, very common, and Alzheimer's is the most common cause of cognitive decline, ultimately dementia. And by definition, this means that you amyloid plaques in the brain and
Dale bredesen tau tangles.
So those are the two main pathological hallmarks of Alzheimer's. But as you see, that doesn't tell you why you it, it just is something you look the brain, and of course, you can get something that Dale bredesen virtually identical without the amyloid and you can get amyloid without the cognitive decline. So, it's a marker but it's an imperfect one. Dale bredesen, that's a really good point you brought up.
And do you have any thoughts on why there are some people that do have amyloid plaques in
Dale bredesen brain that aren't demented and then some others that just don't seem to handle it?
Yeah, it's a great point. So, here's the thing, the whole world is turning upside down now when it comes to our understanding of Alzheimer's. Dale bredesen been over years, of course, going back to Dale bredesen Alzheimer's publications back in and Dale bredesen, and there Dale bredesen been a good understanding of this disease.
And of amyloid has been for years vilified and there's
Dale bredesen question, it is a neurotoxin. It does have toxic effects. The has been that this is also a protectant.
It's actually something that is made by your brain when you have specific insults. It
Dale bredesen, as Professor Ashley Bush showed a number of years Dale bredesen, it's actually quite a good binder of divalent metals like copper and zinc, and things like that, iron. And Dale bredesen showed a number of years ago, it is also a response to a reduction in trophic support, so you actually get a change Dale bredesen signaling. So, there are Dale bredesen different insults and metabolic changes that lead the Dale bredesen to
Dale bredesen this stuff.
And so I think there's been confusion because it's clear that when you produce it you're at this increased risk for having a degenerative process, but as you indicated, there are many people that produce it and they successfully are protecting themselves, they don't actually have the downsizing. What's Dale bredesen been stated is those who then have inflammation on top of that seem to be Dale ones that do worse, and that's
Dale bredesen very Dale bredesen idea, but really it is a set of things.
And we identified and published, a number of years ago, 36 different factors that all contribute to this, but they actually break down into just a couple of categories. So, any
Dale bredesen of pathogens, anything that's giving you inflammation, whether you have it because you have a leaky gut or because you have P.
And in fact, we think more and more of amyloid as being like napalm. You got the bad guys coming across the border, so you're now going to put down stuff that kills the bad guys, the napalm but in so doing you're going to reduce your arable soil. You're now living in a smaller country, and that's exactly what's going on in the brain, you are downsizing the overall network.
So, that's what we call type 1 or inflammatory or hot Alzheimer's. And I should mention, it turns out ayurvedic physicians from thousands of years ago who recognized dementia that was related to something that was hot, that was abnormal and ultimately inflammatory, as well as
Dale bredesen was related to dryness, which is what we call type 2, where you have decreased trophic support.
It can be nerve growth factor, brain-derived neurotrophic factor, estradiol, testosterone, Dale bredesen, progesterone, thyroid, vitamin D, all of these things are critical to support of synaptogenesis.
So we think of the signaling as being a ratio of synaptoblastic activity where you're actually sending signals to make and store synapses just you think of osteoblastic activity versus synaptoclastic activity where you're Dale bredesen pulling back and you're reorganizing.
And of course, this is going on all the time. You're actively forgetting the seventh song that played on the radio on the way to work yesterday and you're actively Dale bredesen a lot but you're remembering the key things, like where your keys are and where your son is and all that sort of stuff.
And so, there is a change in that ratio in Alzheimer's disease because of type 1 with inflammation or type 2, which we call atrophic or cold, because you don't have the support for those synapses, so you're literally I can either watch all five starve slowly or I can put one in a foster home and feed four," and that's the downsizing Dale bredesen happening when you cannot support the neural network that you And then we have a type that's actually type 1.
And we named it that because Dale bredesen has features of both type 1, inflammatory, and type 2, atrophic.
So what happens is you
Dale bredesen insulin resistance, so you now have a change in signaling that actually occurs because of this chronic high insulin. But of course, Dale bredesen also glycating proteins with But Dale bredesen glycating many proteins, so you get now a response to that as well.
So you have an inflammation in an atrophic and so Dale bredesen why it's 1. And then type 3 turns out to be completely different, and that is a response to toxins. So there is a toxic form, which we call toxic or vile Alzheimer's disease.
In addition, there are people we bredesen type 4 who have
Dale bredesen of a vascular and then type 5, which is more of a traumatic component, but they're really both related to these ones. It's really about, do you have inflammation? Are you fighting something off?
you have trophic support, and are you exposed to specific toxins? Wow, and so in all of these different subtypes of Alzheimer's disease they all sort of have some of the same distinguishing pathological features like amyloid beta plaques, tau tangles between all of them.
So they all have amyloid plaques, they all have, by definition, tau tangles, but the presentation can be different.
Now there are some overlaps, the type
Dale bredesen and the type 2s
Dale bredesen typically amnestic presentations more common
Dale bredesen ApoE4, and that's true for the type 1. Dale bredesen type 3s, the toxic ones are quite different. They often present with a non-amnestic presentation. It's dysfunction, problems with calculation, problems with visual perception, problems with word finding, so-called primary progressive aphasia, all of these things, they are really bi-parietal presentations as opposed to bi-temporal presentations, So these have often been called cortical presentations, which have been noted for years by people like Professor Mario Mendez, to be typical in younger presentations of Alzheimer's and often in ApoE4 negative individuals.
I think I also read one in your papers where you did this metabolic profiling there was a very prominent zinc deficiency in that. Yes, so for reasons that we don't entirely understand
Dale bredesen bredesen, many of the people with the type 3, the toxic sub-type have low serum
Dale bredesen, high copper-zinc ratios, and low triglycerides.
The low triglycerides may turn out to be related to malabsorption, we don't know for yet, but we don't really understand why the people often have these
Dale bredesen copper-zinc ratios.
Yeah, so as, you know, copper and zinc actually are competitive, for example, in their absorption. And so, too much of one actually is often associated with too little of another. And then typically in our society,
Dale bredesen you know, most of us are deficient in zinc.
There are actually about a billion people on Earth is the estimate for zinc deficiency. It's a very common problem because if you have poor gastric acidity, which Dale bredesen common as we age, if you're taking PPIs for GERD, if
Dale bredesen taking something for reflux, you won't absorb the zinc very well, if you have copper piping which most of us do, the copper will often compete with the zinc.
And many people have a little too much copper and a little bit too little zinc. And in fact, Dale bredesen was noted over 30 years ago that people with high copper-zinc ratios tended to have dementia more than those with normal copper-zinc ratios. So does this have something to do with it?
I know there's like over to different enzymes in the body that require zinc.
So does copper then bind to those enzymes and then sort of mess up the function or is that like the theory? The theory is that, as you know, copper is a generator of free radicals. You know, copper can act like iron in that sense. It has a free electron in the Dale bredesen orbital which does not occur with zinc. So in general, as you indicated, in these various enzymes, and it's hundreds, just as you said, it is an important structural component and it has a very specific architecture Dale bredesen the enzymes that it serves, so it is a structural thing in general.
And copper, to my knowledge, doesn't replace that.