Researchers at the University of California have received a refutation of the dominating “amyloid” hypothesis in Alzheimer’s disease, which has recently been called into question due to signs of falsification in the work underlying it. The work was published in the Journal of Alzheimer’s Disease.
The dominant hypothesis for the pathogenesis of Alzheimer’s disease suggests that its symptoms arise from the accumulation of amyloid plaques in the brain. They form when amyloid proteins become insoluble and then stick together.
It is not known exactly how the plaques cause Alzheimer’s symptoms. The authors of a new study found that, most likely, nothing. They analyzed the levels of beta-amyloids in patients who, due to the mutation, form amyloid plaques in large quantities. It turned out that the formation of plaques did not lead to cognitive impairment, as long as patients had high levels of soluble beta-amyloid. Participants were followed up for three years.
The authors suggest that cognitive impairments appear due to the fact that amyloid proteins lose their functions during the formation of plaques. In this case, there is a deficiency of soluble “normal” amyloids necessary for brain function.
Some studies have shown that a decrease in the level of soluble beta-amyloid leads to a deterioration in the condition, which confirms the findings of scientists. Now they intend to test whether the condition of patients will improve if the levels of soluble beta-amyloids in the brain are increased.
Earlier, Gazeta.Ru talked about the drug lekanemab for the destruction of amyloid plaques. As the authors of the new study noted, this drug is one of the few that not only destroys plaques, but also increases the level of soluble beta-amyloid.
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