The Great Alzheimer’s Scam and the Proven Cures They’ve Buried for Billions
Description
STORY AT-A-GLANCE
Alzheimer’s disease is commonly thought to result from abnormal plaque buildup in the brain that gradually destroys brain tissue. Almost all Alzheimer’s research for decades has been directed toward eliminating amyloid, even after the basis for much of this work was shown to stem from fraudulent research
The billions spent on amyloid Alzheimer’s research have only produced three drugs, all of which offer minuscule benefits and severe side effects
In contrast, affordable and straightforward treatments that reduce dementia or the preceding cognitive impairment have been maligned and buried by the medical industry
DMSO for example, has incredible neuroprotective qualities that have spared many stroke and spinal cord injury victims from a life of “incurable” disability. Decades of forgotten research also show it treats cognitive impairment and dementia
This article will review the great amyloid scam and the simple therapies for cognitive decline we’re never told about
Medicine is strongly biased towards adopting biochemical models of disease as this facilitates costly therapeutics being developed for each disease and hence sustains the medical industry. Unfortunately, in many cases, the biochemical approach to disease, at best, can manage symptoms, and as a result, many conditions remain “incurable” while non-patentable natural therapies that can cure them languish in obscurity.
That’s 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 20241), we’ve still failed to make any real progress on the disease. This is particularly remarkable given the vast costs to the country (e.g., last year Alzheimer’s was estimated to cost the United States 360 billion dollars2) and the even greater social costs that accompany it.
The Amyloid Juggernaut
In 1906, plaques (of amyloid) in the brain were identified as the cause of Alzheimer’s disease. As the years have gone by, the majority of research for treating Alzheimer’s disease has been targeted at eliminating these plaques. Unfortunately, to quote a 2022 article:3
“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” disproves the notion cholesterol causes heart disease4) and dig deeper and deeper until they can find something to continue propping up their ideology (e.g., cholesterol reducing statins provide almost no benefit for heart disease while having significant side effects yet continue being pushed on patients).
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 pivoted to defending their failed hypothesis was due not to amyloid clumps, but rather toxic parts of it (oligomers) and a Nature 2006 paper appeared which identified a previously unknown toxic oligomer, Aβ*56, and provided proof that it caused dementia in rats.5
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.6 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.”
The Amyloid Scandal
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 Western Blots (and therefore erroneous assessments of what oligomers were present within research subjects’ brains).7 As he explored the topic further, he discovered other papers within the Alzheimer’s literature had been flagged for containing doctored Western Blots.
Note: Western blots, used to test for proteins, are one of the few easily detectable forms of research fraud (e.g., we discovered Pfizer submitted fake Western blots to regulators to “prove” their vaccine wo
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