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A bloody brake on myelin repair

In multiple sclerosis, the blood-coagulation factor fibrinogen can enter the brain. It emerges that fibrinogen inhibits the maturation of cells called oligodendrocytes that repair nerve-fibre insulation and maintain neuronal communication.
  1. Klaus-Armin Nave

    1. Klaus-Armin Nave is in the Department of Neurogenetics, Max Planck Institute of Experimental Medicine, 37075 Göttingen, Germany.

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  2. Hannelore Ehrenreich

    1. Hannelore Ehrenreich is in the Department of Clinical Neuroscience, Max Planck Institute of Experimental Medicine, 37075 Göttingen, Germany.

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Multiple sclerosis (MS) is a debilitating neurological disease in which the body’s immune system destroys the myelin sheath that provides electrical insulation for nerve fibres. Myelin repair subsequently fails owing to a lack of new myelin-producing cells called oligodendrocytes, and this contributes to an irreversible loss of neuronal projections called axons. Why oligodendrocyte precursor cells (OPCs) located at sites of MS-related tissue damage fail to differentiate into oligodendrocytes has been poorly understood. Writing in Neuron, Petersen et al.1 report that a blood-coagulation factor called fibrinogen (which enters the brain when the blood–brain barrier is damaged in MS2) puts a brake on OPC differentiation. This insight offers hope for future treatment strategies.

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Nature 553, 31-32 (2018)

doi: https://doi.org/10.1038/d41586-017-08232-2

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