Here’s some good news on a research study done this month that has potential to translate into a treatment strategy for MS. This new study by Katerina Akassoglou, PhD, funded by the US National MS Society shows for the first time that blocking a segment of fibrinogen – a protein essential for blood clotting – reduces inflammation and symptoms in mice with an MS-like disease, apparently without interfering with normal blood clotting.
Multiple sclerosis occurs when the immune system attacks the brain and spinal cord, damaging the myelin that insulates and protects nerve fibres. Brain cells known as “microglia” participate in this attack and are activated when the blood brain barrier (BBB) – the lining of cells that should protect the brain from intruders – breaks down. As the BBB breaks down, a blood protein called “fibrinogen” leaks into the brain. In addition to its known role in blood clotting, evidence is growing that fibrinogen also participates in the immune response that goes awry in MS. Dr. Akassoglou’s team has uncovered evidence that fibrinogen directly activates microglia, and has developed a method of inhibiting fibrinogen in mice without compromising its clotting capabilities.
Dr. Akassoglou’s team genetically engineered mice in which fibrinogen and Mac-1 did not interact, and found that inducing EAE in these mice resulted in less myelin damage and less severe disease. They then administered a small fragment of fibrinogen – which blocks binding of normal fibrinogen to Mac-1 – to mice with an MS-like disease after the first attack of paralysis. This form of fibrinogen does not block the protein’s interaction with blood platelets, and so would not interfere with clotting. Compared with untreated mice, activation of microglia decreased, myelin damage diminished dramatically, and the treated mice recovered faster and did not experience further relapses. This study highlights the potential of a novel strategy for inhibiting the immune attack in MS and improving symptoms.
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