This is a CD22 protein selected from 3,000 candidates. It stimulates the work of microglia – the “cleaning system” of the brain. Perhaps one day an attack on this protein will help cure Alzheimer’s disease and other neurodegenerative diseases.

With age, the performance of the brain decreases, but the exact mechanisms of this process are still unclear. According to the neurobiologist Tony Wyss-Korey, one of its causes may be changes in microglia — immune brain cells. Among other things, microglia works as a purification system, absorbing waste products of metabolism and spent proteins. In an aging brain, its effectiveness decreases.

It is likely that this process contributes to the age-related extinction of cognitive functions and the development of neurodegenerative diseases. This assumption is supported by the fact that some of the genes associated with Alzheimer’s disease in the brain are active only in microglia. In addition, an abnormal expression of genes in microglia is characteristic of a number of such diseases.

Researchers from Stanford University, whose work is investigated by Science Daily, found a way to “fix” the brain cleaning system. To begin with, they studied how genes affect the ability of microglia to phagocytosis – the capture and digestion of molecules.

The work was done tremendously: scientists consistently “turned on” and “turned off” about 3,000 genes to understand how each of them affects the intensity of phagocytosis.

In a parallel experiment, the team determined which of these genes are more active in the microglia of the hippocampus of young mice, comparing them with older individuals.

Surprisingly, comparing the results of two researchers, the team received only one gene CD22, which suppresses phagocytosis and significantly changes its activity with age. His “shutdown” returned the “cleaning system” to normal.

In the following experiment, it was found that the concentration of CD22 protein in old mice is three times higher than that of their young relatives.

Since CD22 is a surface protein, it can be acted on with antibodies. That is what the team did. On one side of the mouse hippocampus, the researchers introduced antibodies to CD22, and on the other, similar but unable to bind to this protein. In addition to the antibodies, myelinated trash labeled with a fluorescent label was pumped into the hippocampus.

After 48 hours, the concentration of “garbage” was much lower on the side where antibodies to CD22 were injected. Similar results were obtained if myelin was replaced with beta-amyloid and alpha-synucleins, which are associated with Alzheimer’s disease and Parkinson’s disease, respectively.

Continuous injections of antibodies within a month reversed the intellectual extinction of old mice. In the tests for memory and training, the treated individuals were superior to their relatives from the control group.

The human genome also contains the CD22 gene, which makes it a promising target for the fight against neurodegenerative diseases. However, it should be remembered that not all therapeutic methods, confirmed in mice, will definitely work for humans.

Developing an effective drug against Alzheimer’s disease is not easy due to the difficulty of diagnosing this disease in its early stages. However, in the near future, this fatal illness can be identified by a blood test – or even by voice. Bill Gates has already invested in the relevant technology.

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