A study claims that a protein known as fibrinogen that is known to aid in forming blood clots may also set off scar development in the brain and spinal cord. Study authors discovered that fibrinogen carries an inactive factor that may trigger when it enters the brain following an injury, thereby provoking brain cells to form a scar.
Scars in the brain or spinal cord may obstruct connections between nerve cells and frequently keep injury patients from attaining complete recovery. A basic question in studies of damage to the central nervous system has apparently been the origin of the first indication for scar development.
In this study, a group of neuroscientists headed by Katerina Akassoglou, PhD, of the Gladstone Institutes at the University of California, San Francisco, apparently observed the molecules in the bloodstream.
Akassoglou commented, “Our study shows that a blood clotting factor is an important player in glial scar formation.”
Present treatments to enhance nerve cell regeneration following injury seem to concentrate on diminishing present scar tissue. This new outcome proposes that repressing these blood proteins could be a way to prevent scars from even forming.
Following a traumatic injury in the nervous system like a stab wound or stroke, fibrinogen seemingly dischrages from impaired blood vessels into the brain and scar tissue starts to form. This procedure isolates the injured region but also averts nerve cells from reconnecting and interacting with one another. Rewired nerve cells are claimed to be necessary if a patient is to recover normal function.
To find out what function fibrinogen plays in scar formation, the study authors utilized a mouse model of brain trauma. When fibrinogen was efficiently eliminated from the blood stream, the mice appeared to have severely smaller scars following injury. The authors discovered that fibrinogen carries a dormant kind of scar-inducing substance known as TGF-ß that turns ‘on’ when it seems to run into local cells in the brain. When the brain pathways linked to TGF-ß were obstructed, scars apparently didn’t form.
Jerry Silver, PhD, of Case Western Reserve University, who was unaffiliated with the study, commented, “These new findings offer an entirely new avenue to explore potentially important therapeutic agents that interfere with this interesting function of fibrinogen.”
The expert mentioned that it seems to be the 1st time that a major blood-associated trigger of reactive scar-forming cells has been reported in the literature.
The study was published in the Journal of Neuroscience.