Indeed, the blood-clotting protein can work as a signaling protein and trigger signals that block development of oligodendrocytes, the cells that produce myelin. This not only stops myelin production but also prevents the brain from repairing and rebuilding the protective myelin layer that is destroyed during the autoimmune-inflammatory process.
“We found that fibrinogen stops adult stem cells from transforming into the mature cells that produce myelin,” said Dr. Mark Petersen, assistant adjunct professor of pediatrics at UCSF and the study’s lead author. “This blockade could be harmful for regeneration in the brain.”
Inhibition of fibrinogen signals in experimental cells and mice models showed it is possible to reverse the adverse effects of the protein and promote remyelination. These results further support the pursuit of strategies targeting fibrinogen to boost the brain’s regenerative potential.
“Repairing myelin by eliminating the toxic effects of vascular damage in the brain is a new frontier in disease therapeutics,” said Dr. Lennart Mucke, director of the Gladstone Institute of Neurological Disease and professor of neurology at UCSF. “This study could change the way we think about how to repair the brain.”
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