Remyelination is an important therapeutic goal for the treatment of neurological disease and is likely to protect axons from further injury. Human monoclonal antibodies that promote remyelination represent a new class of therapeutics for diseases such as multiple sclerosis (MS), spinal cord injury, neurodegeneration, and stroke. The loss of oligodendrocytes and myelin normally associated with demyelinating diseases such as MS is devastating. During the relapsing-remitting phase of MS, the regression of symptoms is likely due to resolution of inflammation and remyelination, resulting in a return of axon function. All of the antibodies that promote remyelination bind to antigens on the surface of oligodendrocytes, suggesting that these antibodies function through direct stimulation of the myelinproducing cells. Treatment with remyelination-promoting growth factor-like human IgM natural autoantibodies may be an efficacious method for quickly repairing demyelinated lesions and maintaining axonal connectivity. Demyelination predisposes axons to subsequent secondary injury. Rapid remyelination of the preserved axons, induced perhaps by treatment with growth factor-like human monoclonal IgM antibodies directed against myelin antigens, may protect them from further injury and thereby preserve neurological function.
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