An antibody that blocks a blood-clotting factor from leaking into the brain was seen to lessen neuroinflammation and nerve cell damage in mouse models of multiple sclerosis (MS) and Alzheimer’s disease.
Scientists developed an antibody that selectively inhibits the inflammation-triggering capacity of fibrin in the brain — a potential way of treating neurodegenerative conditions — and without limiting its essential work in helping blood to clot.
Fibrin-driven neurodegeneration may be a common mechanism in many neurological diseases, including MS, and targeting it with immunotherapy may be a new way of preventing such damage, the researchers say.
Their study, “Fibrin-targeting immunotherapy protects against neuroinflammation and neurodegeneration,” was published in the journal Nature Immunology.
Chronic activation of the immune response in the central nervous system (the brain and spinal cord) is common to many neurological diseases. Prior research indicates that chronic neuroinflammation and oxidative injury (caused by toxic reactive oxygen species) are key drivers of neurodegeneration in both relapsing–remitting MS (RRMS) and progressive MS.
But little is known about the signals underlying the aggressive and abnormal immune activation that triggers nerve cell damage.
In several neurological disorders, the blood-brain barrier (BBB) — a protective membrane that limits molecules which can move from the blood to the brain — becomes more permeable.
Normally, the BBB only allows the passage of small molecules, fat-soluble molecules, and some gases from the bloodstream into the brain. In many neurological conditions, however, this barrier is disrupted and proteins like fibrin, a key blood-clotting factor, enter.
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