Multiple sclerosis and microglia
Biologists have found out what accelerates the development of multiple sclerosis
Scientists have found that the condition of people with a progressive form of multiple sclerosis worsens due to the reduced activity of the ATG7 gene, which normally causes auxiliary cells of the nervous system to destroy damaged neuron sheaths. The results of the study were published by the scientific journal Science Immunology (Berglund et al., Microglial autophagy–associated phagocytosis is essential for recovery from neuroinflammation).
"Despite the great progress in the study and treatment of multiple sclerosis, about 10-20 years after the onset of the disease, the condition of patients usually worsens. So far there is only one medicine that helps people at this stage. We knew almost nothing about the biological processes that make her symptoms worse," she said. Maya Jagodich, associate professor at the Karolinska Institute (Sweden) and one of the authors of the study.
Multiple sclerosis is an autoimmune disease of the nervous system, in which the cells of the immune system begin to attack the sheath of nerve fibers, the so–called myelin. As a result, the nerves begin to conduct the signal worse and "short out". At first, because of this, the limbs become slightly numb, in the future it can cause paralysis, blindness and death.
According to statistics from the World Health Organization (WHO), about 2.3 million people suffer from multiple sclerosis in the world. There are no full-fledged medications that could completely suppress it yet.
Jagodich and her colleagues have made progress towards the creation of drugs against the most severe form of this disease. They studied how progressive multiple sclerosis develops in mice.
Their experiments showed that the probability of acquiring a progressive form of multiple sclerosis, as well as the rate of its development, depended on the level of activity of the ATG7 gene. It is associated with the so–called autophagy - the process of capturing and processing damaged proteins and other components of cells under stress or lack of food.
Sugar to "fix" the brain
Having discovered the connection between multiple sclerosis and this DNA site, the scientists continued experiments on mice. They were trying to understand exactly how he was connected with the development of the disease. To do this, the researchers began to turn off ATG7 in different types of cells and observe how this affected the aggravation of the symptoms of the disease.
As it turned out, cells of the so–called microglia, an auxiliary tissue that protects neurons from damage, were involved in the development of progressive multiple sclerosis. When scientists turned off ATG7 in their DNA, the condition of the mice deteriorated markedly, and when it was additionally activated, all the symptoms of the disease disappeared.
Subsequent observations showed that this was due to the fact that ATG7 is involved in the removal of damaged myelin fragments and the creation of conditions necessary for the restoration of the protective shell of neurons. Due to a decrease in the activity of this gene, chronic inflammation has developed, which prevents the auxiliary cells of the nervous system from restoring myelin, which ultimately exacerbates the symptoms of the disease.
Scientists have found out that the normal functioning of microglia can be restored with the help of trehalose , a disaccharide that is found in large quantities in the cells of fungi and algae. This compound accelerated autophagy in mouse microglial cells. Thanks to this, about half of the rodents were able to get rid of all the symptoms of multiple sclerosis a few weeks after the start of the experiment.
Interestingly, such a procedure helped only relatively elderly rodents and did not affect the development of multiple sclerosis in young mice. As scientists suggest, this suggests that trehalose affects the activity level not of ATG7, but of genes associated with other forms of autophagy, which gradually stop working in old age. Further study of the nature of the work of this sugar, as Yagodich and her colleagues hope, will help biologists to create a drug that stops the development of multiple sclerosis.
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