TASS, October 16. Scientists have found that the condition of people with advanced multiple sclerosis worsens due to the decreased activity of the ATG7 gene. It forces the auxiliary cells of the nervous system to destroy the damaged membranes of the neurons. The research results were published in a scientific journal Science Immunology.
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“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 drug that helps people at this stage. We knew almost nothing about biological processes, because for which her symptoms are aggravated “- told 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 cells of the immune system begin to attack the sheath of nerve fibers called myelin. As a result, the nerves begin to conduct the signal worse and “close”. 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 worldwide suffer from multiple sclerosis. There are no full-fledged drugs that could completely suppress it.
Yagodich and her colleagues are moving forward on the path to creating drugs for the most severe form of the disease. They studied how progressive multiple sclerosis develops in mice.
Their experiments showed that the likelihood 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 recycling damaged proteins and other components of cells under stress or lack of food.
Sugar to “repair” the brain
Having discovered the connection between multiple sclerosis and this section of DNA, the scientists continued their experiments on mice. They tried to understand exactly how he was associated with the development of the disease. To do this, the researchers began to turn off ATG7 in different cell types 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 worsened markedly, and when it was further 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 creating the conditions necessary for the restoration of the protective membrane 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 aggravates the symptoms of the disease.
Scientists have found that the normal functioning of microglia can be restored with the help of trehalose, a sugary substance 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 symptoms of multiple sclerosis a few weeks after the start of the experiment.
Interestingly, this procedure only helped relatively elderly rodents and did not affect the development of multiple sclerosis in young mice. Scientists suggest that this suggests that trehalose does not affect the level of activity of ATG7, but genes associated with other forms of autophagy, which gradually stop working in old age. Further study of the way this sugar works, Yagodich and her colleagues hope, will help biologists create a drug that stops the development of multiple sclerosis.
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