Recent research uncovers a harmful interaction between amyloid beta and fibrinogen that forms resistant blood clots, contributing to early signs of Alzheimer's disease by damaging blood vessels and synapses, and suggests targeting this complex could offer new therapeutic avenues.
Covid-19 damages the cells lining the smallest blood vessels, choking off blood flow, leading to organ damage, according to a study. The study found that Covid-19 patients had severely high levels of a blood protein called fibrinogen, causing red blood cells to clump together, altering blood flow and directly damaging the endothelial glycocalyx. The fibrinogen-induced red blood cell aggregation and resulting microvascular damage could be the major pathway by which Covid causes organ damage and even death. The team has done exploratory research using therapeutic plasma exchange to remove plasma with high fibrinogen from Covid-19 patients and replacing it with donor plasma that has normal fibrinogen levels.
Researchers at Emory University have discovered that COVID-19 damages the cells lining the smallest blood vessels, choking off blood flow, and that fibrinogen, a blood protein that is extremely elevated in patients with severe COVID-19, causes red blood cells to clump together, altering blood flow and directly damaging the endothelial glycocalyx, a gelatinous protective layer lining the microvessels. The researchers believe that this fibrinogen-induced red blood cell aggregation and resulting microvascular damage could be the major pathway by which COVID causes organ damage and even death. There are presently no medications targeting high fibrinogen in the blood, but the team has done exploratory research using therapeutic plasma exchange.