ReCODE Protocol for Alzheimer's - Dr Dale Bredesen (2025)

By Editorial Team - October 31, 2025

Alzheimer's disease, which is the most common form of dementia, eventually leads to the inability to carry out even the most basic of bodily functions, such as swallowing or walking. It is ultimately fatal, as conventional treatment options are few and universally ineffective.

Dementia vs. Alzheimer’s Disease: What is the Difference?

Like autism among children, Alzheimer's among seniors has reached epidemic proportions, with no slowdown in sight. On the contrary, evidence suggests the trend is worsening. In 2022, Alzheimer's affects more than 6 million Americans,1 and 1 in 3 seniors dies with dementia or other demention. By 2050, Alzheimer's diagnoses are projected to reach 13.8 million.2,3

While the U.S. Centers for Disease Control and Prevention lists the disease as the seventh leading cause of death in the U.S. (4,5), statistics published in the journal Neurology in 2014 revealed Alzheimer's is vastly underreported on death certificates. In reality, the disease likely killed 503,400 American seniors in 2010 (6), making it the third leading cause of death, right behind heart disease and cancer. (7)

The good news is that contrary to conventional claims, there are ways to prevent and even treat this tragic disease — not by drugs, but by diet and other lifestyle changes (Bredesen 2014).

The most compelling research in this field, the work of Dale Bredesen M.D., a neurologist who established an affordable protocol that was proven to successfully treat dementia and has since been replicated by many other physicians (including distant friends of mine). Since many of my references are from his book, I strongly suggest those wishing to learn more read it.

Dr. Dale Bredesen, professor of molecular and medical pharmacology at the University of California, Los Angeles School of Medicine, and author of "The End of Alzheimer's: The First Program to Prevent and Reverse Cognitive Decline," has identified a number of molecular mechanisms at work in Alzheimer's, and created a novel program called ReCODE to treat and reverse it (8).

According to a substack by "a midwestern doctor":

In writing this article, I also conferred with numerous physicians I know who have had success treating dementia (hence why it took so long). Here, I will compare their observations with the most compelling research in this field, the work of Dale Bredesen M.D., a neurologist who established an affordable protocol that was proven to successfully treat dementia and has since been replicated by many other physicians (including distant friends of mine). Since many of my references are from his book, I strongly suggest those wishing to learn more read it.

Note: The protocol used to be called the MEND protocol, but now is called ReCODE.

Related: Best Natural Supplements for Dementia

Dr Dale Bradesen latest book “The Ageless Brain” @Amazon

100-Patient Case Report Sheds Light on Treatment Options

One of Bredesen's publications in 2018 is a case report (9,10) of 100 patients using the ReCODE protocol. He had previously published three case reports, each involving just 10 patients. This fourth case report contains 100 patients treated at 15 different clinics across the U.S., all of which have documented pre- and post-cognitive testing.

Not only did all show improvement in symptoms, some of them also showed improvement in their quantitative electroencephalographs (EEGs). Others who underwent magnetic resonance imaging (MRI) with volumetrics also showed objective improvement.

"By all the criteria, these people showed improvement, subjective and objective," Bredesen says. This is no small thing, as there is no conventional treatment that can reverse Alzheimer's. There have been many drug trials to date, but all have failed to reverse the disease. As noted by Bredesen:

"There are a couple of medications, Aricept, Namenda … but these have a very, very modest impact. The most important thing is their improvement is not sustained. They don't change the outcome of the disease. You get a little bump in improvement, then you go right back to declining.

The most important part of the [ReCODE] protocol … is that the improvement is sustained. You're actually going after the root cause of what is causing the cognitive decline. That's a big difference."

Related: Ivermectin for Parkinson's Disease and Dementia

High-Fructose Corn Syrup Down-Regulates ATP Production

In March 2023, Dr. Richard Johnson, Bredesen, Dr. David Perlmutter and several other coauthors published a paper (Am J Clin Nutr 2023) on Alzheimer’s disease as “a maladaptation of an evolutionary survival pathway mediated by intra-cerebral fructose and uric acid metabolism.”

“It’s really the long-term research of Rick Johnson. You talk about mitochondrial function, about damage to mitochondria. He's talking about a change in signal. They're both important. As he points out, when you get that fructose, your body is literally responding to it saying, ‘Winter is coming. We are going to store fat and we're going to turn down your ATP by about 15%.’

Well, when you're right on the ragged edge of not getting enough energetics, then turning down your ATP by 15% is the last thing you want and is associated with cognitive decline.

Rick put together a whole table looking at all the relationships, changes in PET scans, changes in blood biomarkers. In each of these cases, what happens with fructose is the same thing that happens in Alzheimer's disease.

So again, it comes back to the critical nature of the energetics, whether you're turning them down by taking too much fructose and high fructose corn syrup, which is not to say you can't eat some fruit, it just means you don't want to have massive amounts of fructose.”

Fruit vs. High-Fructose Corn Syrup

Here too, my current views veer a bit. It’s important to understand there is a world of difference between fructose from fruit and high-fructose corn syrup. I used to recommend limiting both sources, but I’ve changed my thinking on this, as fructose from fruit activates pyruvate dehydrogenase, which you need to metabolize glucose from pyruvate to acetyl-CoA in your mitochondria. If that enzyme is not activated, the glucose cannot be used for fuel.

•The key to this riddle is the Randle cycle — This cycle basically acts as a metabolic switch. Your primary fuels are fats and carbs, and the Randle cycle determines how your cells decide which one to burn. When your diet is more than 30% to 35% fat, this switch shifts to fat metabolism, so that you're burning fat in your mitochondria rather than glucose. The glucose instead gets shuttled into glycolysis and any excess goes out into your blood.

•Eating a lot of fruit and a lot of fat at the same time is not a good idea — In essence, fructose by itself is not what’s causing the problem. Rather it’s eating too much fructose in combination with too much fat. If you increase your fresh fruit intake, you also need to lower your fat intake, or else the sugar can’t be used for fuel.

•Individual factors influence carbohydrate tolerance — There are individual variations in metabolic flexibility, toxicity and microbiome that likely contribute to a person’s ability to tolerate increased carbohydrates.

•PUFs may also contribute to metabolic dysfunction — The other point of contention I have is that PUFs also appear to induce torpor (decreased physiological activity marked by a reduced metabolic rate), much like high-fructose corn syrup does. So, I suspect ripe fruit is not going to be a major contributor to dementia.

•Fructose from fruit does not behave like high-fructose corn syrup — In a previous interview with Johnson, he also admitted being surprised that fructose from fruit did not have the same effects as high-fructose corn syrup. Bredesen replies:

“Yes. And it makes perfect sense. The interesting thing to me is we are frugivore (animals that thrive on raw fruits), we are descended from frugivores. The problem we have today, of course, is that our fruit has been bred to have a much higher sugar content. That's the issue.

But the good news is, it retains the wonderful fiber and, as you pointed out, it doesn't give you that effect that high-fructose corn syrup and processed foods give you.”

For a deeper look at the dangers of high-fructose corn syrup and why it should be eliminated from our food supply, read “Why High-Fructose Corn Syrup Must Be Removed from Our Food.”

Methylene Blue, Niacinamide, NAC and Glycine

One treatment adjunct Bredesen favors is methylene blue, which is something I recommend for just about anyone who wants to improve their health and reverse degenerative disease, primarily because it’s so effective at reducing reductive stress.

•Methylene blue supports mitochondrial function — It facilitates electron transfer forward in the mitochondria, thereby allowing ATP production to occur, even if the complexes are damaged.

•Raising NAD+ is important for energy production — NAD+ is oxidized, not reduced, so it facilitates the transfer of electrons forward in the electron transport chain. While there are expensive precursors out there, my favorite is plain old niacinamide, which is incredibly inexpensive yet raises NAD+ effectively.

•Research confirmed that niacinamide helps slow brain aging — For general health, I recommend taking 50 milligrams of niacinamide three times a day. Niacinamide also works synergistically with methylene blue.

•Dementia patients have low glutathione levels — Exposure to mycotoxins or other toxins. Glutathione in its reduced form is less effective, as the oxidized form is needed for optimal function.

•How to make the actual glutathione molecule — You need both cysteine and glycine, so one way to boost your glutathione level would be to take glycine and N-acetylcysteine (NAC).

•Two other ways to get more glycine into your diet — Eating “nose to tail,” not including muscle meat, or taking a collagen supplement or gelatin powder increases your glycine intake. “Nose to tail” refers to organ meats and connective tissues, which are rich in collagen. Collagen, in turn, makes up about one-third of the protein in your body, so it’s incredibly important. About 30% of the collagen and gelatin is glycine, so it’s an excellent source.

Alzheimer's Is a Protective Response to Inflammation

If one were to summarize Bredesen's approach in one sentence, it would be "to improve the ratio between synaptoblastic and synaptoclastic activity, which is the brain's ability to create new synapses versus destroying them." In other words, the treatment allows your brain to create and maintain synapses again. Bredesen explains:

"The molecular biology of this disease shows that what we call Alzheimer's disease is actually a protective response. It's essentially a scorched-earth retreat.

You're pulling back and saying, 'We're not going to let this insult kill us, so we're going to scorch the earth so it (whether it's bacteria or something else) cannot take advantage … of what's there.' You're literally downsizing [your synapses]. As long as those insults are going on, you will be downsized."

Beta-amyloid is a protein that is highly correlated with Alzheimer's. However, all attempts at removing it have failed to improve the condition. Clearly, beta-amyloid in and of itself is not the primary cause, so simply getting rid of it is not the answer.

In Bredesen's paper, he discusses the role of beta-amyloid as an antimicrobial peptide (AMP). Importantly, AMPs are critically important for host immunity. They target organisms such as bacteria, mycobacteria, viruses, fungi and protozoa. He explains:

"Here is the trick. It turns out amyloid beta is really part of the innate immune system. Its antimicrobial effect was first discovered and published by professor Robert Moir and professor Rudy Tanzi at Harvard.

This thing actually has, again, a protective response. Not only is it an AMP, but it also binds some toxins. For example, mercury, other divalent metals like iron and things like that. [Amyloid beta] has multiple effects. It is part of your response to insult.

When you take that into account, you realize it's fine to remove amyloid, but please don't do it before you remove all the insults. We've seen numerous people now who have had the amyloid reduced and gotten worse because the ongoing insults are still there."

In 2019, the drug company Biogen halted its Phase II clinical trial for aducanumab, a drug designed to remove beta-amyloid, and this is the typical story for these kinds of drugs. And then a major trial of yet another approach to amyloid removal, the BACE inhibitor CNP520, was halted because the drug was associated with increased cognitive decline and brain atrophy.11

The Protein Refolding Process Is Impaired in Alzheimer's

About one-third of the proteins your body makes on any given day are misfolded. Thankfully, your body has a mechanism by which those misfolded proteins are refolded. Heat-shock proteins play a central role in this process, and if the misfolding is too severe, the heat-shock proteins help remove them altogether.

In fact, heat-shock proteins are a corollary of autophagy, the process by which your body cleans out damaged organelles. This relates to Alzheimer's, because the refolding process is one of several factors that need to work in order for your brain to function. As noted by Bredesen:

"In all of these different neurodegenerative diseases, whether you're talking about Alzheimer's, Huntington's, Lou Gehrig's disease, Parkinson's disease or Lewy body, they all feature proteins that are aggregated and that are typically misfolded. They are not degraded appropriately.

You lose not only the ability to fold but the ability to degrade these proteins. That is a critical piece. In fact, just recently, an article came out on a common neurodegenerative condition, newly described, which is called LATE, which is limbic-predominant, age-related TDP-43 encephalopathy.

In other words, this is a little bit like Alzheimer's … [LATE] features TDP-43, which is a protein that is involved in numerous things, including protein folding … We lose that [protein-folding] ability as we start to downsize [synapses], as you don't have an appropriate energy, you don't have the appropriate trophic support.

You don't have the appropriate hormonal and nutritional support … When we target ketosis, when we target insulin sensitivity, when we target mitochondrial support, that typically allows you to generate the appropriate ability to refold misfolded proteins …

You can induce the heat-shock response … by doing this combination of sauna and then [going] into the cold and then back to the sauna and then back to the cold …

You are recurrently activating this critical response [by doing that]. There's no question it is going to be important, especially in ALS, but likely in all of the neurodegenerative conditions."

The Link Between Protein Folding and Cell Death

As noted by Bredesen, there are three kinds of autophagy: macro-autophagy, micro-autophagy and chaperone-mediated autophagy. Each offers a slightly different way to repair, remove or recycle damaged organelles within the cell.

Specific proteins, for example, can be targeted for chaperone-mediated autophagy. Bredesen recounts findings of research he did to ascertain the linkage between protein folding and programmed cell death (apoptosis, where the entire cell is killed off and removed):

"If you fail to reform these [misfolded proteins], you literally activate an entire system that initially stops producing more protein. It's basically saying, 'We're not keeping up with this. We're going to shut this down.' It attempts to refold. Then it attempts to destroy the proteins if it can't refold them.

Then ultimately, if it cannot … keep up … it literally activates programmed cell death through specific caspases … This is something where you want to intervene upstream; understand why this is happening. And then if you're unable to keep up with this, now, at least increase your heat-shock proteins so that you can refold. In this case, you prevent the induction of programmed cell death."

Unfortunately, a vast majority of people do not have well-functioning autophagy, for the simple reason that they're insulin-resistant. If you're insulin-resistant, you cannot increase your adenosine 5' monophosphate-activated protein kinase (AMPK) level, which prevents the inhibition of mammalian target of rapamycin (mTOR), and mTOR inhibition is one of the primary drivers of autophagy.

The Case for Cyclical Fasting

While autophagy is clearly of critical importance, you don't want to be in continuous autophagy. You also need to cycle through the rebuilding phase. One of the ways in which you can control this is through cyclical fasting. Bredesen typically recommends an intermittent fasting approach.

"You want to use appropriate fasting and an appropriate diet to activate this autophagy," Bredesen says. "We recommend … 12 to 14 hours [of fasting] if you are apolipoprotein E4-negative (ApoE4-negative) … If you are ApoE4-positive, you'd want to go longer — 14 to 16 hours. There's nothing wrong with doing a longer fast …

The reason we suggest longer for the ApoE4-positives [is because] if you are ApoE4-positive, you are better at absorbing fat. It tends to take longer to enter autophagy …

Typically, we recommend it about once a week. But again, a longer fast once a month is a good idea. It depends a lot on your body mass index (BMI). What we found is people who have higher BMIs respond better to this fasting early on. They're able to generate the ketones.

If you lose both the carbohydrates and the ketones, you end up [feeling] completely out of energy … We are very careful when people are down below 20 on their BMI, especially the ones 18 or below. We want to be very careful to make sure to cycle them [in and out of ketosis] once or twice a week …

These are the ones where, often, exogenous ketones can be very helpful early on … Measure your ketones. It's simple to do. We want to get you into, ultimately, the 1.5 to 4.0 millimolar [range for] betahydroxybutyrate. That is the goal."

Test Your Ketones

So, to recap, while dementia patients with excess weight tend to respond favorably to cyclical fasting, at least initially, underweight patients may experience cognitive decline, as they're simply too underweight to produce ketones in response to the fasting. For those who are underweight, Bredesen recommends using a ketone supplement such as medium-chain triglycerides (MCT) oil.

If that doesn't bring you into the desired ketone level (1.5 to 4.0 mmol), or if it's adversely affecting your low-density lipoprotein (LDL) particle number, he might recommend exogenous ketones — either ketone esters or salts. "We'd like to look at your LDL particle number and use that to titrate, to make sure that your LDL particle number is not too high," he says.

To test your ketones, I recommend KetoCoachX.12 It's one of the least expensive testing devices on the market right now. Another good one is KetoMojo. KetoCoach, however, is less expensive, the strips are individually packed and the device is about half as thick as KetoMojo's, making it easier to travel with.

Energy Demands Are Not Met in Neurodegenerative Diseases

Nutritional ketosis, in which your body produces endogenous ketones (water-soluble fats), is important for all neurodegenerative diseases, but it's not a complete cure-all. Bredesen explains:

"What we've come to realize from the research over the years is that neurodegenerative diseases, whether Alzheimer's … macular degeneration … Lewy body, Parkinson's or ALS, they all have one thing in common. They are related to specific subdomains of the nervous system.

Each of these has a unique requirement for nutrients, hormones, trophic factors, et cetera … In each case, there is a mismatch between the supply and the demand. For most of your life, you're keeping up with that demand. With all of these diseases, you have a repeated or a chronic mismatch between the support and the requirement.

In Parkinson's disease, it's quite clear. You can create Parkinson's disease simply by inhibiting mitochondrial Complex I. That specific subdomain of motor modulation, which is what Parkinson's is all about, is the thing that is the most sensitive to reductions in mitochondrial Complex I support.

Therefore, when people have this, you need to bring the supply back in line with the demand. A critical way to do that is to supply the appropriate ketosis — the appropriate energy.

Now, if the person is continuing to be exposed to whatever chemicals are inhibiting Complex I — and it's typically … mold-related biotoxins or organic toxins such as paraquat or glyphosate — as long as these are ongoing, you're going to get very temporary relief.

The goal here is both to get rid of what is inhibiting Complex I and to flood the system, to help the system by giving appropriate support for the energetics … With Alzheimer's, we're really talking about a mismatch in trophic support. You've got this ongoing need as you're making neuroplasticity."

Why Late-Night Eating Is Ill Advised

Although I am not ApoE4-positive, I prefer fasting for 16 hours a day, essentially narrowing my eating window to just four to six hours. I also make sure to eat my last meal three to six hours before bedtime. One of the reasons for this advice is because avoiding late-night eating will increase your nicotinamide adenine dinucleotide (NAD+) levels, which are important for a variety of bodily functions.

Importantly, it will also reduce nicotinamide adenine dinucleotide phosphate (NADPH), which is essentially the true cellular battery of your cell and has the reductive potential to recharge your antioxidants. The largest consumer of NADPH is the creation of fatty acids.

If you're eating close to bedtime, then you're not going to be able to use the NADPH to burn those calories as energy. Instead, they must be stored some way. To store them, you have to create fat, so you're basically radically lowering your NADPH levels when you eat late at night because they are being consumed to store your extra calories by creating fat.

Bredesen's protocol includes this strategy as well. He calls his approach "KetoFlex 12/3," because it generates mild ketosis and is flexible diet-wise. It can be done whether you're a vegetarian or not. The 12/3 stands for a 12-hour minimum fast each day, and eating the last meal three hours before bedtime.

Certain supplements, including berberine, resveratrol, curcumin, quercetin and fisetin also boost autophagy, and can be used in addition to the nutritional timing. Bredesen explains:

"Sirtuin-1 (SIRT1) was identified as a critical molecule, both for longevity and has been studied extensively for its effects on longevity, but also for its effects on Alzheimer's disease …

ApoE4 actually enters the nucleus and downregulates the production of this critical molecule, so you can see one of its many effects on Alzheimer's disease. Well, when SIRT1 is made, it is actually made in an autoinhibitory fashion. It's just like having a gun in a holster. It's not active … NAD activates the SIRT1.

So does resveratrol. This is why people take resveratrol [or] nicotinamide riboside. These are both activating this program, which is moving you from … more of a pro-inflammatory approach to a longevity approach — a change in your metabolic pattern. That includes activating things like autophagy and also having an anti-Alzheimer's and a pro-longevity effect ...

[Q]uercetin also has an interesting impact on senescent cells … I think that that's going to turn out to be an important way to impact a number of age-related conditions, including neurodegeneration."

The drawback, and the reason you cannot rely on supplements alone, is that the bioabsorption of these polyphenols, like quercetin for example, is quite low. Oftentimes, you cannot absorb enough to get the full benefits.

Limit Electromagnetic Field Exposures

There's also convincing evidence showing electromagnetic field exposures (EMFs) such as that from cellphones and Wi-Fi play an important role. Bredesen agrees, and recommends his patients limit such exposures. In summary, EMFs activate your voltage-gated calcium channels, allowing the release of excess nitric oxide and superoxide in the cell, resulting in the creation of peroxynitrite.

Peroxynitrite causes similar damage to your DNA as ionizing radiation. It also damages your stem cells, mitochondria, proteins and cell membranes. Poly-ADP ribose polymerase helps repair DNA damage by extracting an adenosine diphosphate (ADP) molecule from NAD. Approximately 100 to 150 NAD are required to repair a single DNA break.

While this process works quite well, problems arise when continuous DNA damage requiring continuous PARP activation occurs, as this ends up decimating your NAD+ level. Bredesen adds:

"This is a critical area. The big problem we've had with this so far is that we can measure your NF-κB activation; we can measure your status of hormones, nutrients, magnesium, on and on and on. Typically, with our approach, we measure 150 different variables.

There is no simple way to measure the effect of EMF on a given person's nervous system. I look forward to the day when we can do a test and say, 'Aha. This person has 27.2 on their effects on their voltage-gated calcium channels because of EMFs.' Because then we'll really be able to alter that.

For now, the best we can say is — just as we go after biotoxins and chemotoxins — [EMF] is a physical toxin. The best we can say is, 'Minimize that to the extent you can.' You can certainly measure the exposure. We just don't have a good way yet to measure its effect on your brain."

Randomized Trial Launch Aims to Track and Reverse Cognitive Decline

For starters, his team has published another proof-of-concept paper and is launching a randomized, controlled trial at six sites — Hollywood, Florida; Nashville, Tennessee; Cleveland, Ohio; and Sacramento, Oakland and San Francisco in California.

•The trial will assess biological aging, brain aging and epigenetics — The researchers will use newer blood tests that weren’t available even a few years ago, including phospho-tau 181, phospho-tau 217, A-beta 42 to 40 ratio, glial fibrillary acidic protein (GFAP) and neurofilament light polypeptide (NF-L). “A couple of these are not commercially available yet, so we're doing these as research, but they will all become commercially available,” Bredesen says.

•Early detection and monitoring without a PET scan — Currently, phospho-tau 181 and A-beta 42 to 40 ratio are commercially available, allowing individuals to get an idea of where they stand without necessarily needing a PET scan.

•Tracking improvements and reversing cognitive decline — According to Bredesen, “More importantly, you can follow it as you improve. Prevention is key, but also reversing cognitive decline, which we were the first to do ... We've seen it again and again, when you're doing the right things, when you're attacking the important drivers of the process, you see [reversal].”

This trial represents a major advancement in the ability to monitor and address cognitive decline, offering new hope for prevention and reversal of neurodegenerative processes.

Valuable Tests to Detect Early Signs of Cognitive Decline

Several key tests can provide early insights into brain health, helping to detect neurological changes long before symptoms appear:

•GFAP (Glial Fibrillary Acidic Protein) test — While nonspecific, this test is a valuable tool for detecting brain changes associated with astrocytosis. Astrocytes respond when there’s a problem in the brain, so it can give you a heads-up that something is afoot up to 10 years before symptoms become apparent. “The good news is if it's normal, you're in pretty good shape. So you want to know that going forward,” Bredesen explains.

•Phospho-tau 181 and phospho-tau 217 — These are specific tests for Alzheimer's changes related to the death of neurons.

•Genetic testing for APOE status — Genetic testing is important to ascertain how many copies of the APOE ε4 gene you might have. “That's an [important] piece,” Bredesen says. “Everybody should know their APOE status.”

•Hormone and toxin testing — Assessing hormone levels and screening for toxins, including mycotoxins and heavy metals, provide additional insights into factors that may contribute to cognitive decline.

Where There’s Smoke There’s Fire

According to conventional thought, elevated tau and beta-amyloid are causative factors in Alzheimer’s, but Bredesen’s research suggests otherwise, arguing that these proteins are responses and mediators rather than root causes.

The flawed logic of targeting tau and beta-amyloid — Bredesen explains:

“This is a little bit like saying, ‘There's some smoke there. If we just blow away the smoke, then the house is not going to burn down.’ It makes no sense. The key thing to know is that [tau and beta-amyloid] are responses and mediators.”

Alzheimer’s is caused by multiple upstream contributors — While mitochondrial dysfunction is a well-known factor, many other contributors play a role, including:

Inflammation
Infections (particularly in the mouth)
Insulin resistance
Leaky gut
Reduced blood flow and oxygenation
Diminished mitochondrial function

Alzheimer’s is fundamentally a network insufficiency — The brain contains about 500 trillion synapses, and when environmental and metabolic stressors weaken this network, cognitive function begins to decline. As a result, tau and beta-amyloid emerge, not as primary drivers but as mediators that amplify the damage.
Amyloid is an excellent biomarker but a terrible therapeutic target — Dr. Lee Hood and Dr. Nathan Price, authors of “The Age of Scientific Wellness,” emphasize that while amyloid can indicate disease presence, targeting it therapeutically is ineffective, a conclusion supported by clinical data.
The failure of Lecanemab and what works better — Bredesen criticizes the FDA’s recommendation to approve Lecanemab. “Lecanemab doesn’t make you better, it doesn’t keep you the same, it slows the decline by 27%. That’s it,” he pointed out.
Other interventions performed better in clinical trials — These include ketones alone, extra virgin olive oil, combined metabolic activators (such as carnitine and nicotinamide riboside) and protocols targeting energetics and inflammation.
Bredesen’s protocol shows the best long-term results — He states, “We’ve got people now who have sustained their improvement for more than 10 years. So, it’s sad that this drug has been recommended for approval.”

Bredesen’s Approach to Preventing and Treating Alzheimer’s

According to Bredesen, supporting energy and reducing inflammation in the brain are the two most important factors to prevent and treat Alzheimer’s. Basics that all of Bredesen’s patients implement include:

•Dietary intervention — Bredesen recommends a plant-rich, mildly ketogenic diet, with a good omega-3 to omega-6 ratio, no dairy, no grains and no simple carbs. “That's the approach that has worked the best,” he says. “We call that KetoFLEX 12/3.”

•My concerns about polyunsaturated fats (PUFs) — In the interview, I counter some of Bredesen’s dietary recommendations, as he still recommends PUFs. I’m convinced all omega-6 PUFs need to be kept low, below 2% or even 1% of daily calories, for optimal health.

I strongly suspect people with dementia need to be even more cautious, as linoleic acid (LA) appears to be the biggest dietary source of all the drivers of Alzheimer’s, including inflammation, oxidative stress, mitochondrial dysfunction and dysfunction in electron transport chain such that you cannot efficiently produce ATP.

I’ve written extensively on the ins and outs of this, so for more information, listen to the interview and/or review “Linoleic Acid — The Most Destructive Ingredient in Your Diet.”

•Reevaluating omega fat intake and extended keto — I’m also not convinced that the omega-3 to omega-6 ratio is as helpful as commonly suggested since you cannot counter the damage caused by omega-6 fats simply by taking more omega-3. On top of that, most omega-3 supplements, primarily fish oil, are worthless because they’re synthetic and rancid to boot, so making sure you’re getting high-quality omega-3 is an essential factor.

Lastly, since this interview, I've come to appreciate the importance of carbs for brain health, including simple carbs from whole fruits, and the drawbacks of long-term keto. So, please understand, Bredesen's dietary recommendations are his own, based on his research, and do not necessarily reflect my own views.

•Exercise — Bredesen is seeing particularly good results with KAATSU (blood flow restriction training) and exercise with oxygen therapy (EWOT).

•Sleep optimization — Sleep apnea is a common problem that unquestionably contributes to cognitive decline, as it reduces oxygen to your brain and raises adrenaline while you're sleeping.

“Sleep is a huge area in and of itself,” Bredesen says. “Patient zero, the first person we treated back in 2012 who reversed her cognitive decline beautifully, she's now over a decade in on this, doing great continually. She's now in her late 70s.

One of her issues was poor sleep and, of course, one of the things that was addressed. Getting at least an hour of deep sleep and at least an hour and a half of REM sleep is very helpful ... Poor sleep gives you more amyloid. It's just a marker, but it's a marker of things that aren't so good, and unfortunately, amyloid then gives you poorer sleep.”

•Additional strategies — Other important approaches include stress reduction, brain training, detox and targeted supplementation.

The other part of Bredesen’s program is customized to each patient, as many have undiagnosed chronic infections, for example, that need to be addressed.

•Oral pathogens can invade the brain — Common infections include P. gingivalis and T. denticola, which work their way into your brain from your oral microbiome, herpes simplex and human betaherpesvirus 6A (HHV-6A).

•Herpes viruses are linked to Alzheimer’s — The entire family of herpes viruses is associated with changes in the brain and neurons. HHV-6A in particular is associated with the brain degeneration seen in Alzheimer's.

•Chlamydia pneumoniae and tick-borne infections pose a risk — Chlamydia pneumoniae is also highly troublesome, as are all tick-borne infections, including Borrelia, Bartonella, Babesia and Anaplasma.

•Infections overstimulate the innate immune system — All these infections put your innate immune system into overdrive and need to be quenched. As noted by Bredesen, COVID-19 and Alzheimer’s are “both innate immune system mismatches with the adaptive system.”

You're not clearing the pathogen, so you've got this continued onslaught of cytokines. In the case of COVID, you die from the acute cytokine storm, whereas in Alzheimer's, you die from cytokine drizzle. “It's a long-term cytokine problem,” Bredesen says.

Precision Medicine Program to Launch

Bredesen is also part of a team launching a Precision Medicine Program at the Pacific Neuroscience Institute in Santa Monica, California. The program will work to prevent and treat chronic conditions at all stages, but will focus on getting people in for prevention and early treatment.

Alzheimer’s progresses through four stages — Bredesen explains that Alzheimer’s disease develops gradually, moving through distinct phases: “When you get Alzheimer's, you go through four stages. You go through a presymptomatic phase, and you go through subjective cognitive impairment (SCI) that lasts on average 10 years. For these areas, prevention and treatment are pretty much 100% effective. We can prevent, and we can reverse virtually every time people are in SCI.”
Mild cognitive impairment (MCI) is a late stage of Alzheimer’s — Despite its name, MCI is not mild; it signals significant disease progression. “MCI is the next. It's too bad it's called mild cognitive impairment. It's like telling someone they have mildly metastatic cancer. It's a relatively late stage of Alzheimer's disease. Still, in our trial, we had 84% of those people improve,” said Bredesen.
Reversal is possible, but harder in later stages — While some dementia patients improve with treatment, success rates decrease as the disease progresses. “The final stage is dementia. And we still see some people with proof of dementia improve. But the farther you go, the harder it is to get them all the way back. So, we encourage everyone, please come in early. We've had people go from MoCA [Montreal cognitive assessment] scores of 18 to 30, which is fantastic, from demented to normal. We've had people go from zero to 9. But we've never seen anyone yet be able to go from zero MoCA, which is end-stage Alzheimer's, to perfect 30 ...”
Even small improvements are life-changing — Bredesen recalls a case where a woman with end-stage Alzheimer’s regained independence, even though full recovery was not possible: “A guy wrote me a nasty note a couple years ago, saying ‘How dare you tell people that if they're too far along, they shouldn't get on this protocol? My wife had a MoCA score of zero. She's in a nursing home. We used the protocol that you developed, she only went up a little bit, but her symptoms were so much better.’ She could dress herself, she could speak again, she could engage.”
The best outcomes occur with early intervention — While later-stage patients still see benefits, starting treatment early offers the greatest chance of full reversal. Bredesen noted: “So I don't say there's a limit, but it is much harder below 16. You can get some dramatic subjective improvements. And again, we've seen people go from 15 to 27. So, it does happen, it's just that it’s harder the longer you wait, which is why we encourage everyone to come early. If everybody would come in in those first two phases — prevention or SCI — dementia would be a rare problem.”

On a related note, revelations have called into question long-standing Alzheimer’s research. To learn more about how flawed studies may have misled the scientific community, read “Landmark Alzheimer's Study Retracted After Evidence of Data Manipulation.”

More Information

There's no decline in sight for Alzheimer's, at least in the foreseeable future, so it would behoove most people to just assume you're headed for it and take action now, regardless of your age, to prevent it. When it comes to Alzheimer's, prevention is surely far easier than trying to treat it once it has set in. As noted by Bredesen:

"This is all about prevention and early reversal. Those are the people where we see virtually 100% response. This is why I think there needs to be a global effort to decrease the burden of dementia. We're just now starting a clinical trial. We've been trying to get institutional review board (IRB) approval for years …

It has finally been approved, so we're starting a trial with Dr. Ann Hathaway, Dr. Deborah Gordon and Dr. Kat Toups, who are all seeing patients. We're very excited to see what the trial will show with this approach. Because certainly, anecdotally, we're hearing it all the time.

As you mentioned, we just published a paper a few months ago on 100 patients who showed documented improvement … I'm convinced we could, today, if everyone got an appropriate prevention, make this a very rare disease."

Bredesen's case report is open access, so you can download and read the full study. His book, "The End of Alzheimer's: The First Program to Prevent and Reverse Cognitive Decline," also provides the details, and would be a valuable reference in anyone's health library.

You can also learn more about Bredesen and his work by following him on Facebook, X.com or visit his website, drbredesen.com. Last but not least, read his book, "The First Survivors of Alzheimer's: How Patients Recovered Life and Hope in Their Own Words," which features first-person accounts from patients diagnosed with Alzheimer's who beat the odds and improved.

Frequently Asked Questions (FAQs) About Alzheimer’s Prevention and Treatment

Q: Can Alzheimer’s be reversed?

A: Yes, Dr. Bredesen’s research shows that addressing lifestyle factors reverses cognitive decline in early stages, particularly in the subjective cognitive impairment (SCI) phase.

Q: Is beta-amyloid the main cause of Alzheimer’s?

A: No, beta-amyloid is a response to brain stress, not the root cause. The real drivers include inflammation, infections, insulin resistance and mitochondrial dysfunction.

Q: Why is fructose harmful to brain health?

A: Excess fructose, especially from high-fructose corn syrup, reduces ATP production and triggers fat storage, which contributes to cognitive decline.

Q: Can infections contribute to Alzheimer’s?

A: Yes. Oral pathogens like P. gingivalis, herpes viruses and tick-borne infections fuel chronic inflammation and contribute to neurodegeneration.

Q: What supplements help support brain health?

A: Methylene blue, niacinamide, NAC, glycine and high-quality omega-3s support mitochondrial function and brain energetics.

Sources and References

Republished from: https://articles.mercola.com/sites/articles/archive/2022/11/20/recode-protocol.aspx

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