American scientists made a surprising discovery about the causes of Alzheimer's disease

 In the course of studying the brains of mice, researchers from Yale University found out that the amyloid theory is still somewhat correct.

Despite decades of time and billions of dollars invested in the study of Alzheimer's disease, the main cause of its development is still a mystery.

For many years, the hypothesis about amyloid plaques was considered the main one. It is their accumulation, according to early research, that plays a central role in the development of dementia.

However, recently it turned out that this theory was a fiction - its author probably falsified the results of research.

In addition, the drug aducanumab, which was developed according to the amyloid theory, turned out to be ineffective.

And yet, amyloids occur in the brains of Alzheimer's patients. A team from Yale University drew attention to this fact. Scientists decided to conduct an experiment on mice to understand what is the matter.

They observed that there were hundreds of axons surrounding each amyloid. Next to them, lysosomes are formed - cell organelles, which in this case perform the functions of garbage bags, holding the products of metabolism.

Lysosomes provoke swelling in the area of ​​amyloid and axons. Scientists believe that it is he who is responsible for the deterioration of the conductivity of the signal responsible for memories.

Using voltage imaging of individual cells, the team was able to show that the quality of the signal was related to the size of the swellings. The latter remained stable for a long time, so it is likely that the neuronal malfunctions were permanent.

"Given the similarities in morphology, organelles, and biochemical composition [of the rarity of edema] in mice and humans, it is likely that the causes of dementia in humans may also be caused by edema," the researchers explain.

The team also found a protein called PLD3 in the swelling. At the same time, mice in which it was absent did not have lysosome accumulation and impaired signal conduction.

In the future, the authors of the study want to analyze this discovery and see if this protein can be destroyed and if this will help to cure Alzheimer's disease.