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Journal Scientist Claims Alzheimer’s Aβ*56 Theory a Fraud

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On July 21, Science released an article titled “BLOTS ON A FIELD? A neuroscience image sleuth finds signs of fabrication in scores of Alzheimer’s articles, threatening a reigning theory of the disease“. Once this article was issued, scientists around the world who study Alzheimer's disease were stunned.

In 1906, Alzheimer, a German neuropathologist, discovered special plaques and tangles in the brain of an Alzheimer's patient. Since then, this mental disorder, called Alzheimer's disease, has been in the limelight.

As we all know, the cause of the disease is always an important topic in the research on a disease. Since the 1980s, there has been an amyloid hypothesis in the field of Alzheimer's disease research that this disease is caused by the precipitation and aggregation of Aβ. Therefore, for decades, scientists have devoted themselves to testing this hypothesis, trying to find a causal relationship between Aβ and Alzheimer's disease, but to no avail.

In 2006, Karen Ashe, a renowned professor at the University of Minnesota, led her student Sylvain Lesné to develop the “number one suspect of Alzheimer's disease”, Aβ*56. This paper caused a sensation in the research field and opened a new chapter in the study of Alzheimer's disease. The article was cited more than 2,300 times, being the most cited of any research paper on Alzheimer's disease in the same period. The conclusions drawn from this paper have become almost a consensus in the field and are part of the common knowledge for medical students.

Over the next 16 years, countless funds, time, and efforts were devoted to this direction. However, most of the research on Aβ*56 has been unsuccessful. This is because researchers have found it very difficult to extract Aβ*56, among whom is Matthew Schrag, a neuroscientist at Vanderbilt University.

Dr. Schrag didn't question the underlying theory at first, but question the claimed effect of the new Alzheimer's drug, Simufilam, to repair the protein and reduce Aβ*56 deposition. During the study, he gradually found doubts about the Aβ*56 theory and contacted Science. Science began a six-month review, hiring authoritative independent image analysis reviewers to join and analyze the images. It turned out that there were over 70 images in the paper that laid out the Aβ*56 theory that had been artificially altered.

Admittedly, the fact that this article was falsified does not affect the amyloid hypothesis. aβ*56 is only a subdivision of the Aβ field, and in addition to Aβ*56, other oligomers such as Aβ*42 and Aβ*40 have been studied. Other biomarkers also exist, for example, there has been evidence linking natural autoantibodies and Alzheimer's disease.

However, many believe that this could become the most egregious case of academic fraud ever committed in the United States. Over the course of 16 years, the efforts of countless medical researchers have been misdirected, and countless patients have volunteered to participate in experiments that have not really advanced research on the disease. This also means that Alzheimer's research has been slowed down by this fraudulent paper for 16 years, and over $1.6 billion in research funding that should have provided a major boost to Alzheimer's research has been wasted.

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