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Molecular biologists have discovered that the rate of development of Alzheimer's disease directly depends on how much of the immune system signal protein interleukin-3 is located in the brain tissues.

The main sign and possible cause of the development of Alzheimer's disease is the accumulation of beta-amyloid protein inside brain cells. It is a fragment of the APP protein, which plays an important role in the formation of synapses – connections between neurons.

Recently, scientists have discovered that some auxiliary brain cells, the so-called microglia, can capture and destroy accumulations of beta-amyloid and other protein debris. This does not happen in the brains of patients with Alzheimer's disease. Scientists are trying to understand why, and also find out how to restore the work of microglia cells.

Cameron McAlpin from Harvard University and his colleagues have found out why the vital activity of microglial cells can be disrupted. In the course of a new study, scientists observed how inflammation develops in different areas of the brain of mice genetically predisposed to the development of Alzheimer's disease. Scientists were interested in what signaling molecules of the immune system could be involved in their development and what consequences they led to.

Inflammation has long been considered one of the main factors in the development of Alzheimer's disease, since it accelerates the death of neurons and a large amount of beta-amyloid appears in the intercellular environment. The accumulation of this protein attracts the attention of microglia and cells of the immune system, which causes inflammation to increase and nerve cells to die even more.

As American biologists have discovered, this process is being suppressed by astrocytes – another type of auxiliary brain cells that protect neurons from damage. They produce molecules of interleukin-3, one of the most important signaling proteins of the immune system, which is responsible for suppressing inflammation in other parts of the body and the growth of certain types of stem cells. Previously, scientists have not found a significant amount of interleukin-3 in the brains of humans or animals.

The observations of McAlpin and his colleagues show that the molecules of this substance penetrate into microglial cells, change their shape and vital activity, and also force them to clean the surrounding space from accumulations of beta-amyloid and other protein debris. The more interleukin-3 was in the brain of rodents, the slower they developed Alzheimer's disease.

Scientists have checked whether this pattern is typical for people. As it turned out, the astrocytes of carriers of Alzheimer's disease really produced a large amount of interleukin-3. In the maximum concentration, it appeared in those patients who resisted dementia the longest.

The researchers hope that further research will help to learn the mechanism of action of interleukin-3 on microglia and understand how to make its cells more actively clear the brain of fragments of beta-amyloid. The answers to these questions, in turn, will help to create the first effective drugs for Alzheimer's disease, McAlpin and his colleagues summed up.

The article was published in the journal Nature
© AP Photo/Dake Kan

Source: ITAR-TASS,  sci-dig.ru