title: Mechanisms and Medicines for Remyelination.
abstract: Demyelination of central nervous system axons, associated with traumatic injury and demyelinating diseases such as multiple sclerosis, causes impaired neural transmission and ultimately axon degeneration. Consequently, extensive research has focused on signaling systems that promote myelinating activity of oligodendrocytes or promote production of new oligodendrocytes from oligodendrocyte progenitor cells. Many receptor systems, notably including growth factor receptors and G protein-coupled receptors, control myelination. A number of recent clinical trials target these receptor signaling pathways.
authors.affiliation: Department of Physiology and Biophysics, University of Washington, Seattle, Washington 98195; email: mab@uw.edu.
authors.forename: Mark
authors.initials: M
authors.lastname: Bothwell
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D003711:Demyelinating Diseases / Q000188:drug therapy*; D006801:Humans; D008565:Membrane Proteins / Q000187:drug effects; D009419:Nerve Tissue Proteins / Q000187:drug effects; D011494:Protein Kinases / Q000378:metabolism*; D020794:Receptor Protein-Tyrosine Kinases / Q000378:metabolism*; D043562:Receptors, G-Protein-Coupled / Q000378:metabolism; D000074586:Remyelination / Q000187:drug effects* / Q000502:physiology*; D015398:Signal Transduction
chemical_list: D000911:Antibodies, Monoclonal; C482293:LINGO1 protein, human; D008565:Membrane Proteins; D009419:Nerve Tissue Proteins; D043562:Receptors, G-Protein-Coupled; D011494:Protein Kinases; D020794:Receptor Protein-Tyrosine Kinases; C000625770:opicinumab
keywords: growth factors; oligodendrocytes; receptors; signal transduction