Neurologist proves: Alzheimer’s is curable

An American neurologist has developed a therapy for Alzheimer’s disease: It brings the mental decline to a standstill even reverses it. This approach only fails when the disease is far advanced. He has already saved hundreds of victims. Big Pharma dreads him; Wikipedia hides him.

by Dr.Harald Wiesendanger– Klartext

Background journalism instead of court reporting.
Independent. Uncomfortable. Incorruptible

Instead of leaving it to pharmaceutical companies to banish the Alzheimer’s nightmare, we should expand animal welfare: It must be extended to unfeathered bipeds. As with all diseases of civilization, what is needed above all is humane attitudes that are appropriate to the species to overcome the dreaded neurodegeneration finally. A US neurologist has developed a spectacularly successful treatment concept for this purpose. Not only hundreds of individual cases but also clinical studies confirm it. It is an example of how urgently the world needs a new health culture that frees it from the grip of business interests.

No, one really cannot accuse Wikipedia of having something against Bredesen’s. It pays tribute to a ski jumper, a soccer player, a Nordic combined athlete, a pastor, a businessman with this surname. But one of all people is missing: the American neurologist Dale E. Bredesen. The world owes him a spectacular breakthrough, undoubtedly worthy of a Nobel prize, in the treatment of what is probably the most feared ailment: Alzheimer’s disease. This insidious neurodegeneration is considered incurable. The strange gap in the virtual “world memory” suggests two things: the silent person is seriously disrupting the business interests of those who pull the strings behind the editing of the online encyclopedia, and nothing defamatory can be attached to it.

Conversely, this Bredesen damages the reputation of pharmaceutical-heavy conventional medicine immensely. Because its limits are more evident in hardly any other disease, it has been 116 years since Alois Alzheimer (1864-1915), a German psychiatrist and neuropathologist, first described the dementia disease named after him. He already found in the brains of those affected, in addition to large areas of dead nerve cells, extensive deposits, plaques, of sticky balls of protein, mainly beta-amyloids. Since then, the amyloid hypothesis has prevailed in Alzheimer’s research: almost dogmatically, it clings to the assumption that these plaques are causing the terrible mental deterioration. It is, therefore, necessary to find a patentable pharmaceutical measure that dissolves these plaques or, at some point in their causal history, intervenes in such a way that they do not form in the first place.

An incomparable indictment

Multi-billion research funds have flowed into this approach, and over 50,000 specialist articles have been devoted to it. How many cures has he created so far? Zero. An incomparable indictment. A number of substances are known that deliver encouraging results in test tubes and animal experiments. But as soon as they are tested on humans, they disappoint. By mid-2021, over 400 clinical trials had failed. 99.6% of all candidates turned out to be failures. “Currently approved drugs,” summarizes the American Alzheimer’s Association, “cannot stop or slow down the progression of the disease.” “for a limited time”, usually accompanied by severe side effects. Furthermore, Alzheimer’s disease progresses relentlessly in millions of sufferers – killing everyone statistically between 1.5 and 8.5 years after the onset of impairments.

“Something must be totally wrong here,” thought Bredesen. “It’s like our space rockets invariably explode on the launch pad.” (1)

Not one disease, but three – with 36 factors involved

Bredesen, Professor of Molecular and Medical Pharmacology at the University of California, has now dedicated more than three decades of his academic career to getting to the bottom of the mystery of Alzheimer’s. The doctor has been researching it since 1989: initially with dying brain cells in the test tube, as well as with genetically manipulated test animals that develop symptoms similar to Alzheimer’s. He analyzed confused fruit flies with “Alzflymer” and forgetful transgenic mice with “Mouzheimer.”

After a decade of basic research, Bredesen realized how misunderstood Alzheimer’s was. He discovered how this insidious disease develops. Also, he saw through why all previous efforts to get at her failed so miserably. And he realized how to avoid them, stop them, and defeat them.

Like everything that makes up our mind, our memory is based on a huge network under our skullcap. Over 100 billion nerve cells, neurons form it. Each one is connected to others by nearly 10,000 synapses. This results in a network of almost 1,000,000,000,000,000 connections in total – one quadrillion.

Each neuron has to register somehow and process what is going on in its environment. To do this, it has thousands of receptors: protein molecules that it forms deep inside and then brings to the surface. Most receptors are specialized for a specific job: some detect sex hormones, others vitamin D, still others the happy messenger dopamine. They then instruct the cell to respond appropriately. To do this, they trigger a variety of biochemical reactions. Each receptor does this many billions of times a day.

A receptor called p75NTR caught the particular attention of Bredesen’s team. It encountered him in the basal forebrain, a brain region particularly affected by Alzheimer’s. Its function is to bind to itself neurotrophins: “nerve nutrients”, after the Greek word meaning. When such a bond is formed—which makes neurotrophin the “ligand” of the receptor, as biochemists call it—it signals the cell to maintain and strengthen existing connections and make new ones. However, if this ligand is missing, a veritable suicide program starts: the synapses dissolve, the cell dies.

Is there a molecule that can prevent neurotrophins from binding to their receptors – by taking their place?

It is exactly what amyloid-beta achieves.

Typically, this act of sabotage is not bad but makes sense and is desirable. Cells must die to make way for new ones—perhaps when they are damaged and therefore unable to do their job—and this on-the-fly remodeling is constantly taking place within us. By the time you finish reading that one sentence, more than five million of your white blood cells will have committed suicide—and been replaced by as many new ones. Without mass cellular suicide, Bredesen points out, “we would have webbed fingers (because they wouldn’t break down), a brain that outgrows the skull (because malignant cells survive instead of committing suicide), and many other problems. (2) As such, amyloid-beta is not a villain per se, but usually serves a healthy purpose.

As a result, Alzheimer’s does not develop because a pathological biological process is taking place – but because a vital, protective reaction is getting out of hand. The defense mechanism kicks in when threats become too numerous, too severe, too stubborn, or too chronic: persistent inflammation, poisoning, or nutrient deficiencies.

Then “the brain also resorts to chronic, numerous, stubborn and violent defense strategies – to such an extent that a limit is crossed and the defenses damage the body.” (3) The interplay of dismantling and new construction, devastation and regeneration device out of balance because there is too much amyloid-beta traveling around the brain and attaching itself to receptors, blocking trophic, growth-promoting bonds.

But where does the amyloid excess come from? The search for clues led Bredesen to a molecule appropriately called amyloid precursor protein, APP for short. Amyloid precursor protein. Consisting of 695 amino acids lined up like pearls, it is quite an impressive size. APP is also a receptor but in a superior position. It responds to not just one specific molecule in the cellular environment, but dozens, including many that appear to be linked to Alzheimer’s: estrogen, testosterone, thyroid hormones, insulin, vitamin D, pro-inflammatory molecules, insulin, the “longevity molecule” sirtuin, SirTA. Bredesen compares APP to a chief financial officer who receives constant status reports from specialized accountants – simple receptors: How often and by what have they been activated? The APP boss adds the inputs and takes stock before deciding: Are the available resources sufficient to nourish, model, and rebuild the widely scattered synapses?

If so, the APP receptor docks onto a molecule called netrin-1, which floats past the cells. It then sends the neuron a signal that causes it to continue doing its job. Molecular scissors, called proteases, now cut APP at a specific point. The cuts generate two peptides: sAPPα and αCTF. Bredesen calls them “the constructive duo”: they help maintain synaptic connections, encourage the growth of neuron “fingers” that reach out, and block the suicide program. In short, they are anti-Alzheimer actors.

But what if the APP receptor doesn’t grab netrin-1 or other trophic molecules—and grabs amyloid-beta instead? Then the proteases cut it at three specific points, and four peptides are formed: sAPPβ, Jcasp, C31 – and, 40 to 42 amino acids long, amyloid-beta. They form the “destructive quartet.” It plays a vital role in the process of decay that underlies Alzheimer’s: Brain synapses are lost, the connecting part of the neurons shrinks, and cellular suicide begins.

A vicious cycle is set in motion: cleavage of APP produces amyloid-beta, which binds to APP and causes it to produce more amyloid-beta. Bredesen compares: “Like a tiny vampire, amyloid-beta bites the APP receptor and thereby creates another tiny vampire.” (4)

“I bet you got the point,” Bredesen writes: “To lower your risk of Alzheimer’s, you need to minimize the production of the Alzheimer’s-causing quartet and maximize production of the Alzheimer’s-inhibiting duo.”

What does it depend on which inner program runs – the sustaining, constructive, or the destructive?

Bredesen sees it as wrong to look for the one decisive cause to synthesize a pharmaceutical product tailored to it. In his book The End of Alzheimer’s – published in 2017, a year later also in German translation – he identifies no fewer than 36 factors that may be involved in the fateful APP snippets starting and not stopping: hormonal imbalances and oxidative ones Damage from disturbed intestinal microbiota, excessive blood sugar levels, vitamin D deficiency and gliosis, scarring in the brain from glial cells, up to a high hs-CRP value, an inflammatory marker.

The 36 Alzheimer’s “holes” in the neuronal “roof” result from impacts from three directions. And so Bredesen doesn’t see Alzheimer’s as one disease – for him, there are three. (5) Although they often occur together and their symptoms are similar, they are based on different biochemical processes: (1) inflammation; (2.) Poisoning, for example, by heavy metals or toxins from mold and bacteria; (3.) poor supply of nutrients and other molecules that support synapses.

Why does conventional medicine fail miserably here? Because, as usual, at best, it temporarily alleviates a little of the typical signs of the disease. But it doesn’t fix the root cause. There is more than one, at least 36 are involved. “Pharmaceutical entrepreneurs are like roofers who are called to a house that has been devastated by baseball-sized hailstones,” says Bredesen. “The storm punched dozens of holes in the roof, which the owners plan to have repaired. But the roofers were fixated on a single hole. Maybe they carefully sealed this hole with tar to not rain anymore. Unfortunately, however, they did not take care of the other 35 holes.” (6) And so the house continues to fill up with too much rainwater.

Personalized, involving the whole person: this is the only way to heal

As a trained specialist in internal medicine and neurology, Bredesen was not satisfied with laboratory research. From the very beginning, he was concerned with nothing less than a comprehensive concept that would successfully treat, or even better prevent, the most feared ailment of our time. “Nothing is more important than improving the lives of patients,” he says. (7) He sets the bar high: For him, “success” does not just mean alleviating, slowing down, delaying – but bringing to a standstill, reversing, permanently healing.

When dozens of factors with different weights can be involved, a personal risk profile is required first of all. For each patient, it must first be determined which physiological parameters play a decisive role in his or her case. “Cognoscopy” is what Bredesen calls the entirety of the examinations that have to take place. It includes blood tests, a metabolic profile, an MRI of the brain, and genetic testing. It looks for inflammation and infection, vitamin deficiencies, and hormonal imbalances. She checks parameters such as insulin levels, body mass index, immune status; she examines the microbiome and the permeability of the intestine (“leaky gut”), the oral flora, the blood-brain barrier. “In people with cognitive symptoms such as memory disorders, ten to 25 laboratory values ​​that are related to brain function are often not optimal,” Bredesen noted. “Anyone who has no symptoms yet, but is at risk, usually has three to five suboptimal values.” (8)

And this results in a sophisticated, personalized therapy concept, individually tailored to each person seeking help. Bredesen calls it “ReCODE,” an acronym for reversal of cognitive decline. (9) No two treatments are the same. To stay with the picture: every hail-damaged roof has many holes of different sizes, in different places. The type and cost of the repair work are then determined accordingly. A hole is tight when the laboratory value in question returns to the normal range. The redevelopment aims at nothing less than “reversing cognitive decline”. (10)

What can and must be done to seal the 36 “Alzheimer’s holes”? Do those affected and those at risk need 36 different pharmaceutical creations to be taken at the same time, regardless of questionable interactions and side effects?

It’s much easier, less risky, more promising – and cheaper. To this end, Bredesen recommends seven “core strategies” that reduce the risk of Alzheimer’s, increase resistance and optimize brain functions. (11) They include

  • a mostly plant-based ketogenic diet, high in fat, moderate in protein, and low in carbohydrates. The focus should be on wild-caught seafood and grass-fed eggs. Things to avoid include gluten, processed foods, and polyunsaturated fats, also known as PUFAs, found in low-quality cooking oils and trans fats. Each day should include a long fasting interval of at least 12 hours, preferably 16 to 18. Bredesen also advises taking specific dietary supplements based on the respective laboratory values;
  • an exercise program for outdoors and indoors; avoid sitting for long periods;
  • sufficient restful sleep;
  • Stress management, with meditation and regular breaks for deep conscious breathing;
  • regular brain training;
  • maintain social contacts;
  • Avoid toxins.

It all sounds complicated, but it boils down to a simple message: We can prevent and defeat Alzheimer’s in the same way as any other civilization disease – through a comprehensively healthy lifestyle.

From the lab to practice: does ReCODE work?

After two decades of research, Bredesen finally wanted to prove that his concepts actually work in patients in clinical studies. But twice, in 2011 and again in 2018, examination committees rejected his applications as “unscientific.” (12). Finally, the design of a study must be established before it begins; one cannot only decide in the meantime how the test subjects are to be treated. In addition, only a single variable should be put to the test at a time – not a whole bundle of components at the same time.

Disasters rarely come alone: ​​denied approval prompted a multimillionaire philanthropist to turn off the money supply, and an Alzheimer’s Foundation also stopped funding. And this made the study project unfinanceable.

And so, for years, Bredesen had to limit himself to case reports on Alzheimer’s patients; He published treatment results in 2014, 2016, and 2018.

And they had it all.

His “patient zero” (13), Kristin’s name was 65 when cognitive disorders set in. When she drove on the freeway, she got lost. She no longer knew which entrances and exits to use; even on routes, she knew very well. She no longer understood the information that was important for her work. Writing reports and submitting them on time was too much for her. She could no longer remember telephone numbers, not even simple numbers such as house numbers or the digits on her license plate number. She was finding it increasingly difficult to remember what she had just read; if she had reached the bottom of a page, she had to start again at the top. She called her pets by the wrong name. She had to find light switches in her own home that she had turned on and off for years.

Kristin tried to ignore these symptoms for two years, even though they kept getting worse. Finally, she consulted a doctor. He diagnosed dementia and stated there was nothing he could do for her.

On the recommendation of a friend, Kristin found Bredesen in 2012. Hours of conversations convinced her to get involved with his ReCODE program. Three months later, she called him, almost euphoric: she could hardly believe how her mental abilities had developed. “She was able to work full-time again,” reports Bredesen. (14) “Driving without getting lost and remembering phone numbers with ease. She hasn’t been this good in years, she assured me.” Five years later, now 73, Kristin was still following ReCODE. She also held a full-time job, traveled the world – and remained symptom-free.

Clinical study confirms hundreds of case reports.

Kristin was not an isolated case. In 2014, Bredesen reported in Aging, the leading journal on aging research: He reversed memory loss in 9 out of 10 Alzheimer’s patients who underwent ReCODE for 5 to 24 months. (By the tenth, the disease had progressed too far.) (15)

Two years later, in June 2016, Bredesen’s team reported ten other successfully treated Alzheimer’s patients in the same specialist journal. (16) In May 2018, it presented a collection of 100 such joyful cases. (17)

Bredesen can give hope even to those who are worried about the Damocles sword of a hereditary predisposition. Anyone who carries a gene variant called ApoE4 increases their risk of Alzheimer’s drastically, from the usual 9% to 30% to well over 50%. (18) But even if a DNA analysis confirms the suspicion, there is no reason to despair. Fate can be averted; the sooner, the longer, the more consistently one follows Bredesen’s recommendations.

Several hundred patients have now gone through the ReCODE program. The hissing balance confirms Bredesen’s optimism. Only in a few exceptions – at a very late stage, when too many neurons and synapses have already been lost – does cognitive decline remain irreversible after the causes have been eliminated. Otherwise, Alzheimer’s can be prevented and even cured: during the symptom-free phase, which can last a decade; during what neurologists call “subjective cognitive impairment”—it can last for several years; and even during the mild to moderate phase, when there are already more or less clear limitations that are already reflected in neuropsychiatric tests.

Implementing ReCODE 100% requires iron discipline, and Bredesen makes no secret of that. For example, consistent Alzheimer’s therapy includes “never eating sugar and other simple carbohydrates, including bread, pasta, rice, crackers, cakes, sweets; Grains, dairy, factory foods.” (19) On the other hand, how serious is giving up unhealthy treats when the alternative is to idly accept spiritual self-destructiveness? How strict you should be with yourself depends on the stage of the disease. With only slight, occasional dropouts, permanent, greatest possible self-control would be unnecessarily masochistic – and even counterproductive as a source of stress.

In 2019, Bredesen finally got the green light to carry out a prospective study (lat. prospectivus: forward-looking), i.e., one in which – in contrast to the case report, which summarizes the past – the result has not yet occurred, but lies in the future. How the investigation went and what came out of it were first made public in May 2021 as a preprint. (20) It included 25 participants, between 50 and 76 years old. They all had been diagnosed with “pre-Alzheimer’s” – mild cognitive impairments – or early stages. Bredesen’s team tested each patient for risk factors such as inflammation, insulin resistance, nutrient and hormone deficiencies, cholesterol, specific pathogens, exposure to (bio)toxins, and genetic abnormalities. Subsequent treatment lasted nine months. She followed personalized protocols.

The extremely promising result: In 21 study participants, i.e., 84%, the dementia improved significantly; one showed no change, only three deteriorated mentally. Several cognitive tests demonstrated the improvements. Imaging procedures such as MRI showed that the brain shrinkage that typically occurs with dementia did not happen.

Bredesen published an even more extensive follow-up study, this time with 255 patients, shortly after that, in September 2021. (21) He compared the values ​​of three blood analyses and cognitive tests before the start of the study and two months and one year after the end of the study. This time, the success rate was slightly lower: “Neither the extent of improvement nor the proportion of patients who made progress matched the results of the previous study,” admits Bredesen. (22) He attributes this to the fact that the doctors who advised and instructed the test subjects were less experienced this time and less familiar with ReCODE.

In his latest book, The First Survivors of Alzheimer’s, out August 2021, Bredesen tells the wondrous story of seven people who reversed their mental decline by following the ReCODE protocol. Not only did they survive—they regained a whole life, deep relationships, meaningful work.

The End of Alzheimer’s: The First Program to Prevent and Reverse Cognitive Decline

Pointers for those affected and their families

Bredesen offers detailed instructions for those affected and their relatives in a “practice book” published in 2021.

The German physician and molecular geneticist Dr. Michael Nehls. Since 2011, the former genomics researcher and biotech entrepreneur has published several books (23) on the behavioral changes necessary for healthy aging; he presents his own theory of how Alzheimer’s develops and, based on this, develops a prevention strategy.

A list of 16 doctors, non-medical practitioners, nutritional therapists, health advisors, and coaches who follow Bredesen’s treatment protocol can be found here. According to Dr. Nehls offer, another 60 doctors and therapists who use Alzheimer’s therapy are listed here. Bredesen has personally trained several hundred ReCODE practitioners from the USA to Australia; by 2017, there were already around 450. (24) A Google search for “Bredesen Certified Practitioner” currently returns over 34,000 entries.

Demente’s “world memory.”

The printouts of the entries dedicated to Alzheimer’s disease in the German and English Wikipedia editions are an impressive 35 or 54 pages long. (25) How many words do they have for Bredesen in it? Not a single.

As can be read in the wiki “Talk”, a user suggested six years ago to finally add a reference to Bredesen’s pioneering work in the Alzheimer’s article: “As far as I know, no one has attempted to contradict it, overturn it or even to criticize it in a meaningful way.” (26) The wiki administrators let this suggestion run dry without justification. If our virtual “world memory” is already suffering from such advanced dementia, one must fear and worry about the spiritual future of humanity.

(Harald Wiesendanger)


(1) Dale E. Bredesen: Die Alzheimer-Revolution: Das erste Programm, um Demenz vorzubeugen und zu heilen, mvg Verlag. München 2018, 336 Seiten, S. 15

(2) a.a.O.,S. 75

(3) a.a.O., S. 34

(4) a.a.O., S. 89

(5) a.a.O., S. 113 ff.

(6) a.a.O., S. 95

(7) a.a.O., S. 23

(8) a.a.O., S. 132

(9) Rao RV, Kumar S, Gregory J, Coward C, Okada S, Lipa W, Kelly L, Bredesen DE: „ReCODE: A Personalized, Targeted, Multi-Factorial Therapeutic Program for Reversal of Cognitive Decline“, Biomedicines 9 (10) 2021, PMID: 34680464; PMCID: PMC8533598,

(10) ebda., PDF S. 1

(11) ebda., PDF S. 4, 10 f.

(12) Bredesen: Die Alzheimer-Revolution, s. Anm. 1, S. 102 ff.

(13) a.a.O., S. 22, 29 ff.

(14) a.a.O., S. 31 f.

(15) Bredesen DE u.a.:„Reversal of cognitive decline: a novel therapeutic program“, Aging 6 (9) 2014, S. 707-17, PMID: 25324467; PMCID: PMC4221920,

(16) Bredesen, D.E.; Amos, E.C.; Canick, J.; Ackerley, M.; Raji, C.; Fiala, M.; Ahdidan, J. „Reversal of cognitive decline in Alzheimer’s disease“, Aging (Albany NY) 8/2016, S. 1250–1258,

(17) Bredesen, D.E.; Sharlin, K.; Jenkins, D.; Okuno, M.; Youngberg,W.; Cohen, S.H.; Stefani, A.; Brown, R.L.; Conger, S.; Tanio, C.; et al. „Reversal of Cognitive Decline: 100 Patients“, Journal of Alzheimers Disease & Parkinsonism 8 (5) 2018, S. 1–6,

(18) Bredesen: Die Alzheimer-Revolution, s. Anm. 1, S. 19 ff.

(19) a.a.O., S. 300

(20) K Toups, A Hathaway, D Gordon, H Chung, C Raji, A Boyd, BD. Hill, S Hausman-Cohen, M Attarha, WJ Chwa, M Jarrett, DE Bredesen (2021): „Precision Medicine Approach to Alzheimer’s Disease: Successful Proof-of-Concept Trial“, medRxiv preprint 11. Mai 2021,

(21) Rao RV, Kumar S, Gregory J, Coward C, Okada S, Lipa W, Kelly L, Bredesen DE: „ReCODE: A Personalized, Targeted, Multi-Factorial Therapeutic Program for Reversal of Cognitive Decline“, Biomedicines 9 (10) 2021, PMID: 34680464; PMCID: PMC8533598,

(22) ebda. S. 12.

(23) Die Alzheimer-Lüge: Die Wahrheit über eine vermeidbare Krankheit (2017), Alzheimer ist heilbar: Rechtzeitig zurück in ein gesundes Leben (2017), Die Formel gegen Alzheimer: Die Gebrauchsanweisung für ein gesundes Leben – Ganz einfach vorbeugen und rechtzeitig heilen (2018)

(24) Bredesen: Die Alzheimer-Revolution, s. Anm. 1, S. 33.

(25) Abgerufen am 27.1.2022.

(26) „17 Propose inclusion of Bredesen research on reversing Alzheimer’s/MCI and dividing Alzheimer’s in subtypes“,’s/MCI_and_dividing_Alzheimer’s_in_subtypes