Les plaques beta-amyloïdes, cause unique de l’Alzheimer? Faux:


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The origin (presumé) of Alzheimer’s disease

Beaucoup de gens sont surpris d’apprendre que, malgré des decennie de recherche, il n’y a toujours pas de consensus sur l’origine de cette maladie, et aucun médicament susceptible de lantir son évolution. However, there are 50 million people with dementia in the world, with 10 million new cases each year. Alzheimer’s disease is the most common cause, representing 60 to 70% of cases, according to the World Health Organization. The number of people with dementia could reach 152 million in 2050.

Research on Alzheimer’s has been largely dominated by the amyloid cascade hypothesis, proposed in the 90s. According to this hypothesis, there is only one cause at the origin of the disease. l’accumulation of a protein called beta-amyloid, in the form of “plaques” in the brain. This accumulation leads to a cascade of events that leads to the loss of brain functions, like memory. C’est ainsi que la majoritye des medicos et des expérimentaux visent les plaques amyloïdes – sans grand succes jusqu’ici.

In 2006, the French researcher Sylvain Lesné and his colleagues from the University of Minnesota, published in the journal Nature: un article qui, disaient-ils, apportait une solide prouve en faveur de cette théorie. Chez des mice, ils rapportaient que, when a specific form of amyloid accumulates in the brain, it blocks the transfer of signals between neurons, causes the death of cells and causes a loss of cognitive functions.

Scientific fraud?

Coup de tonnerre en juillet 2022, quand une enquête de la revue Science: reveals that the data at the base of this flagship study may have been falsified (to mid-November 2022, the 2006 study was accompanied by a warning of Nature: disant qu’une enquête est en cours). L’une des spécialists de la fraude scientifique consulted by: Science:, Elisabeth Bik, y declare. “The authors seem to have composed figures and assembled parts of photos from different experiences. The experimental results obtained were perhaps not the desired results, and these data could be modified to… better correspond to a hypothesis.

La recherche de 2006 avait, depuis, servi de justification à plusieurs autres recherches, et au développement d’un médicament, l’Aduhelm, dont l’approbation accélerée aux États Unis, en juin 2021, a été denoncée par plusieurs experts.

According to Frédéric Checler, director of a research laboratory on Alzheimer’s and Parkinson’s diseases in France, et cité dans le journal Le Monde en juillet dernier, “no one has ever succeeded in replicating these results.” [de 2006] “.

Pas de cause unique

Il nuance toutefois. even if this study had to be retracted, it would not mean that the amyloid does not play any role in the disease. Cela confirmerait plutôt qu’on a erré sur son rôle dominant.

Dans la baladodiffusion Ask a Harvard Professor, in 2021, the professor of neurology of this university, Rudolph Tanzi, y était allé d’une métaphore. amyloïde serait à la maladie d’Alzheimer ce que le cholestérol est aux maladies cardiaques. The high levels would be a signal of alarm, before symptoms appear.

Ce chercheur evoquait toutefois d’autres causes pouvant aussi servir de signales d’alarme, et severales experts du domaine s’entendaient depuis longtemps pour dire que rien ne permet de faire des “plaques” la unique cause de la maladie d’Alzheimer. une multitude de facteurs y contributor probably. A page from the National Institutes of Health (NIH), the main research funding body in the United States, lists age-related changes in the brain, as well as genetic and other factors related to the mode of vie.

The problem is that the dominance of the theory of the amyloid cascade has slowed the research on the other factors of Alzheimer’s. The professor of biology and chemistry at the University of Texas at San Antonio, George Perry, spoke in 2021 about the “obsession” for the sole cause of amyloid, in the magazine New Scientist. So far, anti-amyloid drugs have not succeeded in improving the symptoms of the disease.

One of these “other factors” is the accumulation in the brain of the protein called Tau. Normally, it helps to support the structure of neurons, but some modifications can be done in such a way that they agglutinate in the neurons, interfering with their ability to communicate. When the disease develops, the amount of accumulation of tau seems to be correlated with the severity of dementia.

On sait aussi que les gènes jouent un rôle. trois gènes défectueux ont été identifiément comme facteur de risque de l’Alzheimer précoce (celui, more rare, qui survient between 30 et 65 ans); they contribute to the production of amyloid, in a process that is still poorly understood. Other genetic variants are probably still to be discovered, which affect for example the ability to eliminate beta-amyloid from the brain. Plus precisely, le fait d’avoir une version du gene de l’apolipoproteine ​​E: (APOE) augmente le risque de développer la maladie d’Alzheimer.

Finally, research has suggested a multitude of factors that influence the development or evolution of the disease. for example, arterial hypertension, cardiovascular diseases, or even diabetes and obesity.

If it turns out that factors linked to the mode of life are actually in cause, the parallel with the heart diseases would be useful. pour elles, il existe des treatmentes allant des medicos until surgical interventions, but also a set of recommendations allant from changes to l’alimentation until l’exercise physique. Est-ce la piste à suivre pour l’Alzheimer?

Verdict:

The majority of researchers who studied Alzheimer’s disease recognized, bien avant l’enquête de juillet dernier, que la maladie avait de multiple factors encore mal compris. But “obsession” for the only cause of amyloid has hindered progress towards possible treatments.

Photo: Noelle Otto / Pexels

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