Alzheimer’s: Does suspected fraud cast doubt on our understanding of the disease?

For more than two decades, clinical research on Alzheimer’s disease has produced many therapeutic impasses. Some see this as a refutation of the amyloid hypothesis. However, this hypothesis has dominated Alzheimer’s research for a long time. Although controversial, there is strong evidence to consider it scientifically valid. But here it isa particularly thorough investigation published in the newspaper Sciences suspected fraud in an article published in 2006 in Nature. The latter is much cited in Alzheimer’s research. Beyond the ongoing investigation, research suggests that this fraud could undermine the amyloid hypothesis. According to Jean-Charles Lambert, director of research at Inserm, a neuroscientist specializing in Alzheimer’s disease at Lille University Hospital, this is not the case.

A media frenzy

To fully understand what is happening, it is necessary to specify the content of the article that is the subject of suspected fraud. The latter seeks to demonstrate the existence of a oligomer of protein Synthesis of…” data-image=”https://cdn.futura-sciences.com/buildsv6/images/midioriginal/c/2/1/c21d283fdf_50038231_plaques-seniles-amyloid-nephron-wiki-cc -30 .jpg” data-url=”https://news.google.com/health/definitions/biology-amyloid-plaque-11751/” data-more=”Read More”>beta-amyloid that would be associated with cognitive impairment in the animal model: amyloid beta protein *56 (AB*56), according to its dough molecular weight of 56 kilo Daltons. Therefore, it is not the heart of what supports the amyloid hypothesis that is in question, but an additional hypothesis, about one of the oligomers of this protein.

But what is the difference? If this article has been cited frequently, that suggests it was influential, and articles that were based on these results are also good to throw away. This is when you have to take a step back. Jean-Charles Lambert, who is familiar with the Alzheimer’s disease literature, discusses the reasons why this article is highly cited: ” It is a pioneering work in the investigation of toxic oligomers of amyloid proteins and it is above all for this reason that it is cited by other research teams”.

Not so influential results

This is important because it is not so much the methodology as the results that are suspected of being fraudulent: Western Blot images (a biotechnology to separate and identify the proteins in a sample) would have been manipulated to adhere to the initial hypothesis. However, as Jean-Charles Lambert points out, “ no one has been able to reproduce the results of the AB*56 protein. From then on, the results were no longer taken seriously by the scientific community.”

What must be understood is that the AB*56 protein is not the only oligomer studied in the pathogenicity of Alzheimer’s disease. There are others, and the fact that the results for one oligomer are potentially fraudulent does not mean that the others are. Therefore, even less does it imply the fallacy of the amyloid hypothesis. On the other hand, the researchers now better understand why no one was able to replicate the results related to this oligomer.

Financing risks

If this enthusiasm is misunderstood by the general public and the body politic, it could lead to less funding, in an area already suffering from a lack of resources. Indeed, according to a recent Senate report, research in biology and health appears to be underfunded compared to most developed countries. The amyloid hypothesis is certainly not untouchable. We already have expressed doubts about him in Futura and consider alternative hypotheses. However, he must not take advantage of bad arguments and preach for his theoretical parish. If the amyloid hypothesis is false, (honest) scientific work will prove it.

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