The Great Alzheimer's Scam and The Proven Cures They've Buried for Billions

Decades of neglect in understanding the actual causes of dementia have transformed it into one of the most costly diseases in existence.

Oct 07, 2025

• Alzheimer’s disease is commonly thought to result from abnormal plaque buildup in the brain that gradually destroys brain tissue. As a result, almost all Alzheimer’s research has been directed toward eliminating amyloid, even after the basis for much of this work was shown to stem from fraudulent research.

•As such, despite decades of research and billions of dollars spent, this model has completely failed to produce useful results. The costly “groundbreaking” Alzheimer’s drugs only slightly slow dementia progression—at the expense of causing brain bleeding and swelling in over a quarter of those treated.

•In contrast, numerous affordable treatments have been developed for Alzheimer’s disease that target the root causes of the disorder, producing significant benefits at a fraction of the cost and without any toxicity.

•One neurologist, for example, proposed that amyloid serves a protective function in the brain and treats Alzheimer’s by identifying the underlying process causing dementia (which can often be diagnosed through symptoms). Remarkably, despite the method being proven in clinical research, awareness of it or the fact there are completely different types of “Alzheimer’s disease” which require different treatments remains almost nonexistent.

•Likewise, a strong case can be made that impaired cerebral circulation, along with impaired venous and lymphatic drainage, plays a pivotal role in Alzheimer’s disease.

•This article will review the common causes of cognitive impairment and dementia (e.g., cells becoming trapped in a shocked state where they no longer function) along with the forgotten treatments for neurodegenerative disorders—some of which, like DMSO, have extensive evidence supporting their use.

One of the least appreciated aspects of medicine is the numerous frameworks that have been developed to understand how the body works and how to heal it. This, I believe is a result of conventional medicine having successfully branded itself as the one true path to understanding the body and each remaining approach being a “second-rate gimmick,” which at best, can sometimes assume a complementary role in healthcare.

However, if you study those other approaches, you will find each medical system excels at certain types of health problems, while struggling with others, so in many instances, knowing which medical model to jump to can be immensely beneficial to patients.

The modern approach to medicine is heavily biased towards a biochemistry model, where customized drugs are designed to stimulate or inhibit specific molecular targets (most commonly enzymes, frequently cellular receptors or ion channels, and less often, other aspects of the body, such as individual genes or inflammatory messengers). This approach, in turn, tends to excel for specific issues (particularly acute emergencies) but typically struggles with chronic ailments—something I attribute both to target molecules rarely being able to reach broad swathes of the body and partly due to living organisms being designed to adapt to excessive stimulation or inhibition of specific receptors and enzymes within the body.

Yet despite its frequent failures, we continue to rigidly adhere to that model of medicine. This I believe, ultimately is because therapies produced within this framework are highly specific to individual diseases (hence allowing many distinct patentable products), and in many cases (since they can only temporarily shift an enzyme or receptor) do not produce lasting cures—hence requiring perpetual purchases of them and thus recurring pharmaceutical sales.
Note: in many cases, disabling critical enzymes or receptors also creates a myriad of side effects (particularly over time as the body readjusts itself to accommodate this unnatural state).

All of this summarizes why, despite spending an ever increasing amount of money on Alzheimer’s research (e.g., the NIH spent 2.9 billion in 2020 and 3.9 billion in 2024), we have still failed to make any real progress on the disease. Furthermore, we only spend that much money on Alzheimer’s research because of how dire its costs are (e.g., last year it was estimated to cost the United States 360 billion dollars). Sadly, this figure only touches the surface of the social cost (as any relative of someone with Alzheimer’s can attest)—again making it so remarkable we still have not made any progress in the illness.

The Amyloid Juggernaut

The early history of Alzheimer’s research is as follows: In 1906, plaques in the brain were identified as the cause of Alzheimer’s disease, in 1984, amyloid beta protein was identified as the primary component of those plaques, and in 1991, genetic mutations in a protein that gives rise to amyloid beta was linked to inherited forms of Alzheimer’s disease—creating a widespread believe a cure for this devastating disease was at last at hand.

The existing dogma within Alzheimer’s research, hence, became that Alzheimer’s disease results from the buildup of amyloid plaques within the brain, which then cause brain damage that leads to Alzheimer’s disease. As such, the majority of research for treating Alzheimer’s disease has thus been targeted at eliminating these plaques, but unfortunately:

Hundreds of clinical trials of amyloid-targeted therapies have yielded few glimmers of promise, however; only the underwhelming Aduhelm has gained FDA approval. Yet Aβ still dominates research and drug development. NIH spent about $1.6 billion on projects that mention amyloids in this fiscal year, about half its overall Alzheimer’s funding. Scientists who advance other potential Alzheimer’s causes, such as immune dysfunction or inflammation, complain they have been sidelined by the “amyloid mafia.” Forsayeth says the amyloid hypothesis became “the scientific equivalent of the Ptolemaic model of the Solar System,” in which the Sun and planets rotate around Earth.

Note: frequently, when a faulty paradigm fails to explain the disease it claims to address, rather than admit the paradigm is flawed, its adherents will label each conflicting piece of evidence as a paradox (e.g., the French “paradox” clearly disproves the cholesterol hypothesis) and dig deeper and deeper until they can find something to continue propping up their ideology. For those interested, the key misunderstandings about cholesterol, heart disease, and statins are discussed here.

The consistent failure of the amyloid model to cure Alzheimer’s gradually invited increasing skepticism towards it, which resulted in more and more scientists studying alternative models of the disease. Before long, they found other factors played a far more significant role in causing the disease (e.g., chronic inflammation), and by 2006, this perspective appeared poised to change the direction of Alzheimer’s research.

In response, the amyloid proponents adopted the position that the shortcoming of their hypothesis was that the cause of Alzheimer’s was not the presence of amyloid plaques in general, but rather the formation of certain toxic oligomers (smaller clumps of amyloid beta). In turn, as dissent towards the amyloid hypothesis was reaching a critical mass, a 2006 paper (published in Nature) identified a previously unknown toxic oligomer, amyloid beta star 56 or Aβ*56, and provided proof that it caused dementia in rats.

This paper cemented both the amyloid beta and toxic oligomer hypotheses (as it provided the proof many adherents to the theory had been waiting for) and rapidly became one of the most cited works in the field of Alzheimer’s research. Its authors rose to academic stardom, produced further papers validating their initial hypothesis, and billions more were invested by both the NIH and the pharmaceutical industry in research of the amyloid and toxic oligomer hypothesis.

It should be noted that some were skeptical of their findings and likewise were unable to replicate this data, but rarely had a voice in the debate:

The spotty evidence that Aβ*56 plays a role in Alzheimer’s had [long] raised eyebrows. Wilcock has long doubted studies that claim to use “purified” Aβ*56. Such oligomers are notoriously unstable, converting to other oligomer types spontaneously. Multiple types can be present in a sample even after purification efforts, making it hard to say any cognitive effects are due to Aβ*56 alone, she notes—assuming it exists. In fact, Wilcock and others say, several labs have tried and failed to find Aβ*56, although few have published those findings. Journals are often uninterested in negative results, and researchers can be reluctant to contradict a famous investigator.

Sound familiar?

Amyloid Scandals

Fifteen years later, at the end of 2021, a neuroscientist physician was hired by investors to evaluate an experimental Alzheimer’s drug and discovered signs that its data consisted of doctored images of Western Blot protein tests (and therefore erroneous assessments of what oligomers were present within research subjects’ brains). As he explored the topic further, he discovered other papers within the Alzheimer’s literature had been flagged by Pubpeer (a website scientists use to identify suspect studies) for containing doctored Western Blots.

Before long, he noticed three of these papers had been published by the same author and decided to investigate their other publications. This led him to the seminal 2006 Alzheimer’s publication, which like the author’s other works, contained clear signs of fraud (again illustrating how criminals typically get caught because they repeated the same crime).

A subsequent investigation uncovered 20 papers written by the author, 10 of which pertained to Aβ*56, and many outside investigators, after being consulted, agreed that the images had been manipulated. A co-researcher came forward, stating that he had previously suspected the author of scientific misconduct (shortly before 2006) and not only withdrew his collaboration with the author but also declined to publish a study they had collaborated on, so he would not potentially be implicated in scientific misconduct.

Note: a major concern with the mRNA vaccines was whether they were stable enough to actually produce their intended product. Since Western Blots are used to demonstrate the presence of proteins, they were presented as proof of vaccine efficacy. When reviewing Pfizer’s regulatory submissions, we discovered that their Western Blots had been fabricated (and hence exposed this in January 2023, as, at the time, provable fraud was one of the few things that could derail the mRNA campaign)—but of course, were completely ignored.

The Amyloid Industry

One of the remarkable things about this monumental fraud was how little was done about it. For example, the physician who discovered it notified the NIH in January 2022, yet in May 2022, beyond nothing being done, the suspect researcher was awarded a coveted $764,792 research grant by the NIH (which was signed off by another one of the authors of the 2006 paper).

In July 2022, Science published an article exposing the incident and the clear fraud that had occurred, after which a few other independent voices attempted to draw attention to it (e.g., I did in October 2022). Despite this, the researcher was allowed to remain in his position as a tenured medical school professor. It was not until June 2024 that the 2006 article was retracted at the request of the authors—all of whom denied being at fault and insisted the doctored images had not affected the article’s conclusions (and likewise the amyloid field claimed this fraud had not refuted the amyloid hypothesis). Eventually, on January 29, 2025, during his confirmation hearing, RFK cited the paper as an example of the institutional fraud and wasted tax dollars within the NIH, and a few days later, that researcher announced his resignation from the medical school professorship (while still maintaining his innocence).

All of this, on the surface, is quite strange and illustrates how much the medical field was willing to walk in lockstep to protect the amyloid hypothesis, something I attribute both to how much many researchers have are dependent upon perpetual funding for it and also how profitable the potential amyloid market is (e.g., roughly 7 million adults have it, many of the therapies cost tens of thousands a year and in theory, they must be covered by Medicare, equating to hundreds of billion in annual sales).

Recently, the fate of the failed amyloid drugs appeared to be changing, as a new pharmaceutical (a monoclonal antibody) demonstrated some success in treating Alzheimer’s—something which was treated as revolutionary by the medical community, the pharmaceutical industry, and drug regulators, as all of them had been waiting for decades for a drug like that to emerge. In turn, the first new drug received accelerated approval (which the FDA proudly announced), due to the controversy surrounding the first one. The second received a quiet backdoor approval, while the third was partially approved a year and a half later.

Each year, Chase Bank holds a private conference for pharmaceutical investors, which sets the tone for the entire industry. In 2023 (the first in-person one since the pandemic), its focus (covered in detail here) was on the incredible profitability of the new Alzheimer’s drugs and the GLP-1s like Ozempic (which the FDA has also relentlessly promoted). While much could be said about the jubilation of that private conference, in my eyes, the most crucial detail was that the (widely viewed as corrupt) FDA commissioner was the keynote speaker, and a few days before the conference, had enacted the second backdoor approval.

However, despite the rosy pictures painted around the drugs (which each attacked different aspects of amyloids), they were highly controversial as:

•The FDA’s independent advisory panel, in a very unusual move, voted 10-0 (with one abstaining) against approving the first amyloid drug (which targeted amyloid plaques), then the FDA approved it anyways. In a highly unprecedented move, three of the advisors resigned, calling it “probably the worst drug approval decision in recent U.S. history.”

•That drug was priced at $56,000 a year—making it sufficient to bankrupt Medicaire, which attracted a Congressional investigation and led to each subsequent one being priced roughly half that amount (along with its price later being reduced to match that).

•Brain swelling or brain bleeding was found in 41% of patients enrolled in its studies. Additionally, headaches (including migraines and occipital neuralgia), falls, diarrhea, confusion, and delirium were also notably elevated compared to placebo.

•No improvement in Alzheimer’s was noted; rather one analysis found it slowed the progression of Alzheimer’s by 20% (although this could have been a protocol artifact rather than a real effect).

The second monoclonal antibody (which targeted amyloid precursors) had a slightly better risk benefit profile (only 21% experienced brain bleeding and swelling), and 26.4% reduction in the progression of Alzheimer’s was detected in the trail (which for context, translated to a 0.45 reduction on a scale where a reduction of at least 1-2 points is needed to create an impact which is in anyway meaningful for a patient).

The third monoclonal (which targeted amyloid plaques thought to be more pathologic) was also contested as it caused 36.8% of recipients to develop brain bleeding or swelling, like the other amyloid medications, frequently caused headaches and infusion reactions (e.g., nausea, vomiting, changes in blood pressure, hypersensitive reactions or anaphylaxis) and there were reasons to suspect the trial had overstated its benefits.

Given the controversy around the first two drugs, the third was met with widespread protest, but in a remarkable pivot, the FDA’s new advisory panel, voted unanimously in favor of it, despite it having a very similar mechanism, efficacy and toxicity to the previously unanimously rejected amyloid drug (which they attributed to it having a better trial design and guidelines for usage). It should hence come as no surprise that when the British Medical Journal conducted an independent investigation, they discovered that within publicly available databases, 9 out of 10 members of the advisory committee had significant financial conflicts of interest.
Note: the tenth individual who voted for the drug, the patient representative, did not exist within those databases and, therefore, could not be assessed.

In short, I believe it is fair to say that the amyloid drugs are effectively failed medications, both due to their side effects and negligible benefits. Fortunately, despite the aggressive promotion of them, despite Chase’s best attempts to promote the sector, the market somewhat recognized how bad they were, as the first drug had its price halved. Then it was withdrawn from the market as no one wanted it (making around 5 million dollars total), while the other two have had very modest sales (e.g., 295 million for the most popular one).

From this, three things stand out:

•These drugs consistently damaging brain tissue indicated either that their mechanism of action (triggering the brains immune cells to attach amyloids) would cause those immune cells also to attack the brain or that removing amyloid (regardless of the way it was done) damages brain tissue (suggesting amyloid has a protective effect for the brain) and damages brain blood vessels (e.g., because the amyloids patch vessel walls)—either of which strongly argues against the approach. Curious, I checked, and there indeed is evidence for all three of those occurring (and an active subject of discussion)—yet it has not deterred the usage of this therapy.

•An absolutely absurd amount of money and time has been wasted on this endeavor due to the medical field’s need to find a patentable drug.

•The focus on these lucrative drugs has diverted attention from other treatments that are more likely to help Alzheimer’s patients. In turn, the entire reason I wrote this article is because those treatments do indeed exist, and the harm from withholding them has been incalculable.

For example, after I posted a few articles about Alzheimer’s early in this publication’s history, I had numerous readers reach out to share that coconut oil, or coconut oil-derived MCTs, had significantly improved an ailing relative’s dementia. I checked, and found a randomized controlled trial that over 6 months, found 80% remained stable or improved—which for context, is better than what any of the amyloid drug trials showed, and more importantly, does not cause brain bleeds and costs a lot less than the annual (approximately) $30,000 cost for those drugs. I share this, not to claim coconut oil is the cure for dementia, but rather to highlight just how much the data from these drugs have been overvalued to create a new drug market.

Likewise, very few are aware of a 2022 study that should have revolutionized the entire Alzheimer’s field:

Note: Bredesen’s references for the above chart can be found here, here, and here.

Dale Bredesen’s Discovery

Dale Bredesen is a creative neurologist with a background in functional medicine who spent several years examining the Alzheimer’s question. From it, as detailed in The End of Alzheimer’s, he reached a few pivotal conclusions:

•Amyloid protein is a protective mechanism the brain uses to protect itself from other stressors that endanger brain tissue.

•Rather than there being one type of Alzheimer’s, there are actually three with different symptoms, and it is essential to recognize which type someone has before initiating treatment.

•The brain is designed to be able to adapt to the needs of life, so it is always creating or pruning neural connections and brain cells. Alzheimer’s, in turn, results from the loss of signals that sustain brain cells, and the dismantling of neural connections outweighing the formation of new ones, gradually compounding over the decades.

As such, his formula was fairly straightforward: identify the type of Alzheimer’s someone has, eliminate its causes, and gradually wait for the physiological momentum to shift from neurodegeneration to neurodevelopment.

Most importantly, as the previous chart showed, his model worked. Beginning with a 2018 report of 100 patients from numerous providers whose cognitive decline was reversed by this model, a pilot study (completed in 2022) was able to show these remarkable case reports could be replicated in a controlled manner:

Likewise, he showed these improvements correlated to simple biochemical improvements:

Additionally, in 2024, he published a detailed set of case histories of patients who had remarkable responses to this protocol, and since his protocol was popularized, neurologists around the country he trained have begun administering it, often with significant success.

What Causes Alzheimer’s Disease?

This mirrors the three hats worn by the multitalented molecule, amyloid-beta, which is derived from APP. It is part of the inflammatory response and can function as an antimicrobial agent (thus it is part of your body’s ability to fight infections); it responds to inadequate levels of hormones, vitamins, nutrients, and other supportive (or trophic) factors by downsizing the more expendable synapses; it is part of the protective response to toxin exposure—for example, binding very tightly to metals such as mercury and copper [due to its negative charge].

In Bredesen’s model, there are multiple distinct types of Alzheimer’s disease, reflecting different underlying causes. The original three subtypes have since been expanded to at least five, each representing a different biological driver of cognitive decline. They are as follows:

• Type 1 – Inflammatory: This form is driven by excessive inflammation, often metabolic or infectious in nature. Chronic activation of the immune system—due to factors such as insulin resistance, a poor diet, a leaky gut, or latent infections—leads the brain to engage in protective downsizing by removing synapses and neurons that are less essential for immediate survival. This subtype often presents with classic Alzheimer’s memory loss and typically develops in the sixties to seventies. However, in individuals with substantial genetic risk (e.g., APOE4 carriers), it may appear earlier—in the late forties to fifties, or in the late fifties to sixties for those with a milder genetic predisposition.

• Type 1.5 – Glycotoxic: Sometimes referred to as a hybrid of Types 1 and 2, this subtype arises from insulin resistance and chronically elevated blood sugar. It leads to both inflammatory and trophic deficiencies, and is driven by glycotoxicity and the accumulation of advanced glycation end products (AGEs), which impair cellular function and synaptic integrity. It typically appears in the late fifties to sixties and is especially common in individuals with prediabetes or metabolic syndrome.
Note: the enzyme the body uses to break down insulin (which is nearly always chronically elevated in those who have metabolic syndrome) is the same enzyme it uses to break down amyloid plaques. Likewise, because elevated insulin levels and metabolic dysfunction play such a key role in Alzheimer’s, this has led many to refer to it as “type 3 diabetes.”

• Type 2 – Atrophic: This type is caused by deficiencies in nutrients, hormones, and other factors that provide trophic (supportive) signals to brain cells. These include vitamin D, thyroid hormone, estrogen, progesterone, testosterone, and brain-derived neurotrophic factor (BDNF), among others. The resulting lack of neuronal support triggers a similar downsizing mechanism seen in Type 1. Type 2 tends to emerge about a decade later than Type 1 and may occur alongside it, particularly in individuals experiencing both inflammation and hormonal/nutritional decline.
Note: I believe that in many cases, functional nutritional deficiencies result not from a lack of nutrients, but rather from a lack of fluid circulation that prevents those nutrients from reaching the cells. For this reason, I find that better results are sometimes seen from improving fluid circulation rather than aggressively increasing supplemental nutrition.

• Type 3 – Toxic: This subtype results from exposure to toxic substances that directly damage neurons. Common culprits include biotoxins, such as mold-derived mycotoxins (from water-damaged buildings—which is a huge issue), chronic infections (including Lyme disease), heavy metals (like mercury and lead), and industrial or household chemicals.
Note: the exact infectious agents are a matter of debate. For example, we’ve found that Cytomegalovirus, and Human Herpesvirus 6, can periodically cause cognitive decline, and once an appropriate antiviral is administered, a significant improvement is observed. Likewise, many believe Lyme bacteria within the brain is one of the most common infectious causes of cognitive decline and frequently treat it to address the condition. Bredesen, in his work highlights the importance of Herpes simplex-1 virus, Lyme disease (a spirochete bacterium), P. gingivalis (an oral bacterium), and various fungal infections (mold toxins are notorious for causing cognitive impairment at all ages). Others also emphasize the importance of oral spirochete bacteria, which can travel into the brain.

Unlike Types 1 and 2, which involve more selective and adaptive brain responses, Type 3 causes widespread and often unpredictable neuronal death. It typically occurs earlier in life—often between the forties and sixties—and is less strongly associated with genetic risk factors, such as APOE4. Cognitive decline in this type is frequently accompanied by psychiatric symptoms, sensory changes, or executive dysfunction (e.g., difficulty with math, organization, executive tasks), rather than the more classic early Alzheimer’s memory loss. This type typically cannot be reversed unless the source of toxicity is identified and removed.

Note: I believe some of the most important neurotoxins to avoid are pharmaceuticals, and when I meet elderly individuals who have preserved their mental clarity, many report having largely avoided pharmaceuticals throughout their lives. Some of the most common problematic medications for brain health include certain high blood pressure medications (because they lower cerebral perfusion), statins (as they inhibit the production of compounds essential for brain function), acid reflux medications (which interfere with the absorption of vital brain nutrients—making it critical for everyone to have adequate stomach acid), antidepressants, antipsychotics, benzodiazepines, antihistamines (since, like many sleeping pills, they block restorative sleep), and anticholinergics (such as those prescribed for incontinence).

Additionally, after creating the initial list, he later created two more types:

• Type 4 – Vascular: In this form, chronic restriction of cerebral blood flow—due to factors such as hypertension, atherosclerosis, or small vessel disease—leads to gradual neuronal injury and cognitive decline. This vascular insufficiency deprives neurons of oxygen and glucose, impairing their function and survival. Type 4 often appears later in life (typically in the seventies or beyond) and may overlap with other subtypes. It tends to affect processing speed, attention, and executive function rather than memory alone.

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