Methods are described for treating demyelinating diseases in mammals, such as multiple sclerosis in humans, and viral diseases of the central nervous system of humans and domestic animals, such as post-infectious encephalomyelitis, or prophylactically inhibiting the initiation or progression of demyelination in these disease states, using human monoclonal autoantibodies characterized by their ability to bind structures and cells within the central nervous system. In particular, the methods utilize human monoclonal antibodies selected from the group of sHIgM22 (LIM 22), sHIgM46 cbvHIgM MSI19D10, CB2bG8, AKJR4, CB2iE12, CB2iE7 and MSI 19E5, monomers thereof, active fragments thereof and isolated or synthetic human or humanized autoantibodies having the characteristics of the foregoing. Nucleic acids and DNA molecules encoding the human monoclonal antibodies, or portions thereof, are provided. The invention also extends to the preparation and use of human polyclonal and monoclonal autoantibodies, monomers thereof, active fragments, peptide derivatives and fragments, and analogs, cognates, agonists and the like corresponding materials, and their use in diagnostic and therapeutic applications. For example, the autoantibodies, monomers, fragments, haptens, and peptide equivalents, are useful in the promotion of neural regeneration and neuroprotection, and therapeutic compositions and vaccines containing peptides or antibodies are included and presented.
