The myelination of axons by glial cells was the last major step in the evolution of cells in the vertebrate nervous system, and white-matter tracts are key to the architecture of the mammalian brain. Cell biology and mouse genetics have provided insight into axon–glia signalling and the molecular architecture of the myelin sheath. Glial cells that myelinate axons were found to have a dual role by also supporting the long-term integrity of those axons. This function may be independent of myelin itself. Myelin abnormalities cause a number of neurological diseases, and may also contribute to complex neuropsychiatric disorders.
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I apologize to all colleagues whose important work could not be cited owing to space limitations. I thank S. Goebbels and H. Werner for help with figures, and J. Edgar and D. Dietrich for providing images. I also thank all members of my group as well as D. Attwell, P. Casaccia, J. Edgar, I. Griffiths, O. Peles, J. Salzer, S. Scherer, P. Stys and B. Trapp for discussions. Work in my laboratory is supported by the German Research Foundation (Center for Molecular Physiology of the Brain in Göttingen, SFB/TR43), the European Leukodystrophy Association, the Myelin Project, the German Federal Ministry of Education and Research (Leukonet) and the European Union (Sixth Framework Programme, Neuropromise; Seventh Framework Programme, Ngidd, Leukotreat).
The author declares no competing financial interests.
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