Alzheimer’s disease research over two decades may be based on deliberate fraud that has claimed millions of lives

The suspicion that something was more than a simple mistake in the model that gets nearly all of Alzheimer’s research funding ($1.6 billion last year alone) began with a fight over Simufilam. The drug was pushed into trials by its manufacturer, Cassava Sciences, but a group of scientists who reviewed the drug’s maker’s claims about Simufilam thought it was overstating the potential. So they did what any sane person would do: They bought short positions in Cassava Sciences stock, submitted a letter to the FDA asking for a review before the drug was allowed to go to trial, and hired an investigator to provide some support for the position.

as such Sciences Reports, that was the investigator, a neuroscientist at Vanderbilt University and a junior professor Matthew Schrag, who pushed the entire shopping cart to discover that cassava wasn’t just ineffective. There is good evidence that over the past 16 years, almost everyone has had a wrong idea about the cause of Alzheimer’s disease. because of fraud.

in 2006, temper nature He published a paper titled “Assembling a specific amyloid-beta protein in the brain impairs memory.” Using a series of studies in mice, the paper concluded that “Memory deficits in middle-aged mice ‘directed by accumulations’ a soluble substance calledAβ*56.” This was a specific form of a group known as ‘Toxic oligomers’ that have long been suspected as possible precursors of amyloid plaques. The paper then went on to relate this condition directly to “Cognitive deficits associated with Alzheimer’s disease “independently of other conditions that affect brain aging.”

The study did not come out of nowhere. It seemed to confirm only one of the many hypotheses about Alzheimer’s that had been circulating for many years at that point. After all, the brains of Alzheimer’s patients contain plaques that can sometimes seriously alter the structure of the brain. These plaques contain amyloid. It is not an exaggeration to suggest that these amyloids are the main cause of associated memory loss and dementia. Amyloid causes plaques, plaques damage, and damage causes Alzheimer’s disease. QED.

This 2006 research paper was primarily authored by Professor of Neuroscience Sylvain Lesne and given more weight by the name of the highly respected neuroscientist. Karen Ash, both from the University of Minnesota’s powerful neuroscience research team. It was Ash who produced the genetically modified mice used in the study, which really appear to have Alzheimer’s-like symptoms and which have since been used as the preferred animal models for a generation of treatments. On her website, Ash called Aβ*56 “the first substance ever identified in brain tissue in Alzheimer’s disease research that has been shown to cause memory impairment.”

The results of the study seem to show the amyloid pipeline to Alzheimer’s disease so clearly that even the average reader can understand, and it has become one of – if not the most – influential research papers in all of Alzheimer’s research. Not only has it been cited hundreds of times in other work, but nearly 100 of the 130 Alzheimer’s drugs are now working their way through trials designed to directly attack the type of amyloid found in this paper. Rock neuroscientists, Ashe and Lesné, became wave leaders based on their 2006 research.

What’s curious Shrag When he returned to this primary work were the photos. The images in the paper that were supposed to show the relationship between memory problems and the presence of Aβ*56 appear to have changed. Some of them appear to have been pieced together from multiple photos. wreck He avoided actually accusing this foundational paper of being “fraud,” but it certainly raised “red flags.” He raised these concerns, initially discreetly, in a letter sent directly to the National Institutes of Health (NIH). Only when that letter failed to elicit a reaction shrap his skepticism to others.

Currently Sciences She concluded her own six-month review, during which he consulted with image experts. What they found seems to confirm Schrag’s suspicions.

They agreed with his general conclusions, which cast doubt on hundreds of photographs, including more than 70 in Lesny’s papers. Some of them look like “shockingly stark” examples of image manipulation, says Donna Wilcock, an Alzheimer’s disease expert at the University of Kentucky.

After reviewing the images, molecular biologist Elizabeth Beck said of the research paper, “The experimental results obtained may not be the desired results, and these data may have been changed to…better fit the hypothesis.”

If this fraud turns out to be as widespread as it first appears, the effects will go beyond merely misleading tens of billions of funding and millions of hours of research over the past two decades. Since the 2006 publication, the presence or absence of this specific amyloid has often been addressed Diagnosis Alzheimer’s disease. Meaning, patients who died of Alzheimer’s disease may have been misdiagnosed as having something else. Those whose dementia came about for other reasons may have been dragged under the umbrella of Alzheimer’s disease. And every possible kind of study, whether it’s as bizarre as light therapy or as long-term as nuns doing crossword puzzles, may eventually have results that have been measured with the wrong scale.

In the face of potential fraud discovered by Schrag, it’s not as if the world changed overnight.

Four months after Schrag submitted his concerns to the NIH, the NIH turned around and awarded Lesnie a five-year scholarship to study… Alzheimer’s disease. This scholarship was awarded by Austin Yang, Program Director at the National Institute on Aging of the National Institutes of Health. Yang also happens to be one of the co-authors of the 2006 paper.

Sciences He detailed the work done on image analysis. Other researchers, including a 2008 Harvard paper, noted that Aβ*56 is unstable and there appears to be no sign of this substance in human tissue, making targeting it literally worse than useless. However, Lesné claims to have a way to measure Aβ*56 and other oligomers in brain cells that served as the basis for a series of additional research papers, all of which are now in doubt.

It seems that there is no doubt about it oligarchs It may play a role in cognitive impairment. However, this role may not be nearly as direct or significant as the 2006 and later papers he wrote. Suggest me. It is entirely possible to be specific Aβ*56 . oligomer It may not even exist Outside transgenic Ash mice.

And it seems very likely that over the past 16 years, most research on Alzheimer’s disease and most of the new drugs entering trials have been based on a paper that has, at best, modified the results of its findings to make them appear more conclusive, and at worst outright fraud.

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