The Proven Cures For Alzheimer’s That Have Been Hidden
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) (and one which is now used to smear papers that go against government narratives – Ed) 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.
See more here midwesterndoctor.com
Header image: News-Medical
Please Donate Below To Support Our Ongoing Work To Defend The Scientific Method
PRINCIPIA SCIENTIFIC INTERNATIONAL, legally registered in the UK as a company 
incorporated for charitable purposes. Head Office: 27 Old Gloucester Street, London WC1N 3AX.