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. Yet 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 issuspected fraud on an article published in 2006 in . The latter is extremely cited in research on Alzheimer’s. Beyond the ongoing investigation, the investigation suggests that this fraud could undermine the amyloid hypothesis. According to Jean-Charles Lambert, research director at Inserm, neuroscientist specializing in Alzheimer’s disease at the University Hospital of Lille, this is not the case.
A media frenzy
To fully understand what is happening, it is necessary to specify the content of the article which is the subject of suspicion of fraud. The latter intends to demonstrate the existence of aprotein which would be associated with cognitive decline in the animal model: the amyloid beta protein *56 (AB*56), in accordance with its molecular weight of 56 kilo Daltons. It is therefore not the heart of what supports the amyloid hypothesis that is called into question but an additional hypothesis, on one of the oligomers of this protein.
But what is the difference? If this article has been cited often, that suggests it was influential, and articles that relied 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 literature on Alzheimer’s disease, discusses the reasons why this article is highly cited: ” It is a pioneering paper in research on toxic oligomers of amyloid proteins and it is above all for this purpose 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 to be fraudulent: Western Blot images (ato separate and identify the proteins of a sample) would have been tampered with to stick to the initial hypothesis. Yet, as Jean-Charles Lambert points out, “ no one has succeeded in reproducing the results for 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 concerning an oligomer are potentially fraudulent does not imply that the others are also. Therefore, it even less implies the fallacy of the amyloid hypothesis. On the other hand, the researchers now better understand why no one was able to replicate the results concerning this oligomer.
If this excitement is misunderstood by the general public and by the body politic, it could lead to less funding, in an area that is already suffering from a lack of resources. Indeed, according to, research in biology and health appears underfunded in comparison with the majority of developed countries. The amyloid hypothesis is certainly not untouchable. We already have and consider alternative hypotheses. However, you should not seize bad arguments and preach for your theoretical parish. If the amyloid hypothesis is false, (honest) scientific work will take care of demonstrating it.
What you must remember
- Suspicion of fraud affects several research articles concerning Alzheimer’s disease;
- These articles were influential for their methodologies and not for their results;
- Therefore, the potential fraud, as serious as it is, does not call into question the amyloid hypothesis.