A blood-clotting protein called fibrinogen prevents myelin production and blocks the neuron remyelination repair process in mice, a study finds.
The study, “Fibrinogen Activates BMP Signaling in Oligodendrocyte Progenitor Cells and Inhibits Remyelination after Vascular Damage,” appeared in the journal Neuron. Its conclusions offer new insights and open new therapeutic avenues for multiple sclerosis (MS) and Alzheimer’s disease, among other illnesses.
One common feature of several neurological disorders is the loss of the myelin layer that normally surrounds neurons. Myelin is essential not only to protect the neurons but also to let them process and transmit the electric pulses they use to communicate with each other. When myelin is degraded, neurons can not work properly and they eventually die.
Scientists have tried to better understand what factors contribute to the demyelinating process and how to protect neurons from it.
Attempting to add new insights, a research team led by Katerina Akassoglou, senior investigator at Gladstone Institutes and professor of neurology at the University of California, San Francisco (UCSF), tested if the blood-clotting protein fibrinogen could be involved in MS.
“We thought it might be important to look instead at the toxic environment outside the cell, where blood proteins accumulate,” Akassoglou said in a press release. “We realized that targeting the blood protein fibrinogen could open up the possibility for new types of therapies to promote brain repair.”
In a previous study, the team showed that when fibrinogen crosses the brain-blood barrier it can induce autoimmune responses in the brain, similar to those involved in MS. In this new study, the team revealed that fibrinogen can do much more than that.
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