Oligodendrolysis [Oligodendrolysis; Oligodendro(Gliocyte) + Greek. Lysis Decay, Destruction]

Oligodendrocytolysis is a pathological process of destruction of supporting cells in the brain and spinal cord that support the functioning of nerve cells. A synonym for the term is oligodentolysis. Most often, children under one year old or infants one month old are affected, but in practice the disease can occur in patients of different ages. The term was first introduced by the English neurologist Karl Meine. Describing the degenerative process in the body, the doctor indicated the main source of the lesion - spontaneous necrosis of myelin-forming glial cells (oligodentrogalia).

The prevalence of oligodentrolysis in the world is no more than 2-4% in children. Most cases are diagnosed before six months of age. The pathology affects about 3% of all young children. The peak incidence occurs in the first 6 months of life, after which a persistent improvement occurs, which is considered complete recovery. About 5% of cases of oligodentylosis before one year are fatal. In 9% of these cases, these children die from heart disease due to insufficient blood circulation to the brain. At the same time, children with gliocyte necrosis develop mentally and physically, and subsequent disorders of the nervous system are associated with other factors.

The basis for the development of oligodentalosis is childhood infectious diseases. And also complications against their background:

CMV (cytomegalovirus); Intrauterine infection; Infectious mononucleosis; HSV; AND

Oligodendrolysis [Oligoden-droly-sis; olidogendr(gliocyte) + Greek Lysis] - disintegration of oligodendron glia cells or oligodendron gliocytes, in which the process of loss of substance from a structurally unified and integral nerve cell, after various damages, for example, long-term hypoxic factors, leading to disruption of the functions of nerve cells in an area that does not recover for a long time.

Biological significance: - Function of facilitating axonal growth and myelination of neurons. When axons are pinched around a restored synapse, oligodentric cells (observed, for example, in the case of repercussion in persons who have suffered a spinal cord injury) release protein and glial factors that are capable of activating the activity of ERK-type kinases upon contact with their stimulating factor, which impairs survival and subsequent regeneration nerve cells. Therefore, the content of these cells correlates with axonal activity. Following degeneration of oligodetric cells, excess repairing adhesion factors are released, including cytrienes, fetingamine, pentrandimine or saponins, which reattach myelin around damaged nerve fibers and promote repair. In contrast to myelination of neuron-like cells by neurostimulin (NTZ),