07 November 2017

Fibrinogen inhibits remyelination

Katerina Akassoglou and her group from the Gladstone Institute (USA) have discovered an interesting relationship between myelin repair and plasma proteins.

Myelin is a substance that covers the processes of neurons and creates an insulating layer that protects against damage and increases the rate of transmission of nerve impulses. The destruction of the myelin sheath occurs in serious diseases and conditions: multiple sclerosis, traumatic spinal cord injuries, birth trauma, Alzheimer's disease. Without myelin, nerves are extremely vulnerable to environmental factors, and the pulse transmission rate is noticeably reduced. This leads to sensory and motor disorders, changes in cognitive functions.

For many years, researchers have been trying to shed light on the mechanism of myelin recovery and find out the reasons for its failure, thereby overcoming the currently incurable demyelinating diseases.

The brain responds to damage to the myelin sheath of the nerve by activating its recovery mechanisms. In the central nervous system there are cells capable of restoring myelin – oligodendrocytes. If necessary, their immature progenitor cells migrate to the damaged area and differentiate into oligodendrocytes, whose main function is the myelination of axons of nerve cells. But this process, due to the action of unknown factors, does not bring results. The researchers found that one of them is a violation of the blood-brain barrier. At the same time, plasma proteins enter the central nervous system, including fibrinogen, in the presence of which the process of restoring myelin is completely inhibited.

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In vitro fibrinogen activates bone morphogenetic protein, which is a signal for the process of differentiation of oligodendrocyte precursors into mature forms. An overabundance of signals slows down this process, and remyelination is suppressed.

In vivo, fibrinogen depletion leads to a decrease in active signaling proteins and promotes remyelination.

Regeneration of myelin in brain cells would contribute to the cure of such serious diseases as multiple sclerosis, Alzheimer's disease, recovery after stroke, traumatic brain, spinal cord and birth injuries. As the authors write, this is possible if the toxic effect on the process of remyelination of the fibrinogen protein is excluded by restoring the blood-brain barrier.

Article by Mark A. Petersen et al. Fibrinogen Activates BMP Signaling in Oligodendrocyte Progenitor Cells and Inhibits Remyelination after Vascular Damage published in the journal Cell.

Aminat Adzhieva, portal "Eternal Youth" http://vechnayamolodost.ru based on the materials of Gladstone Institutes: Blood-Clotting Protein Prevents Repair in the Brain.


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