Göttinger Graduiertenschule für Neurowissenschaften, Biophysik und Molekulare Biowissenschaften

Nave, Klaus-Armin, Prof. Dr.

Professor of Molecular Biology, Director at the Max Planck Institute for Experimental Medicine


  • 1987 PhD, University of California, San Diego
  • 1987-1991 Postdoc, The Salk Institute, la Jolla, California
  • 1991 Junior Group Leader, ZMBH, University of Heidelberg
  • 1998 Professor of Molecular Biology (C4), ZMBH, University of Heidelberg



Major Research Interests

We are studying the interactions of neurons and glial cells in the mammalian nervous system with a special interest in the role of oligodendrocytes and Schwann cells, best known as myelin forming cells of the central and peripheral nervous system. These highly specialized glial cells enwrap axons with a multilayered sheath that provides electrical insulation for rapid impulse propagation. However the biology of these axon-glia interactions is complex. Using mouse genetics, originally to study the role of proteins in the myelin architecture and in neurogenetic disorders, we made the unexpected discovery of a novel function of oligodendrocytes, which even precedes myelin in nervous system evolution: the glial metabolic support of axonal conduction, axonal transport and long-term integrity. We determined that oligodendrocytes and Schwann cells take up glucose and deliver lactate, here the product of aerobic glycolysis, to the axonal compartment. This supportive function helps maintaining axon functions especially when ATP demands are increased at higher firing rates, also because access of axons to extracellular metabolites is restricted by myelin itself. Here, the fine architecture of the myelin sheath that we visualize with advanced electron microscopic techniques appears critical. Specialized cytoplasmic connections within the myelin sheath (‘myelinic nanochannels’) must provide a pathway of continuous communication between oligodendrocytes and the encapsulated axon. In neurological diseases, in which myelin is structurally affected or even destroyed, such as in multiple scleroses, leukodystrophies and various peripheral neuropathies, there is invariably secondary axonal degeneration that we propose is caused by the lack of adequate metabolic support. We are investigating the underlying molecular mechanisms of these diseases in detail, using corresponding animal models that we have generated with a range of genetic techniques. A further goal is to understand the role of myelinating glial cells in higher brain functions and psychiatric diseases, which we approach in close collaboration with the Department of Hannelore Ehrenreich at our institute.




Homepage Department/Research Group

http://www.em.mpg.de/index.php?id=34&no_cache=1



Selected Recent Publications


  • Saab AS, Tzvetavona ID, Trevisiol A, Baltan S, Dibaj P, Kusch K, Möbius W, Goetze B, Jahn HM, Huang W, Steffens H, Schomburg ED, Pérez-Samartín A, Pérez-Cerdá F, Bakhtiari D, Matute C, Löwel S, Griesinger C, Hirrlinger J, Kirchhoff F, Nave KA (2016) Oligodendroglial NMDA receptors regulate glucose import and axonal energy metabolism. Neuron 91: 119-32
  • Goebbels S, Wieser GL, Pieper A, Spitzer S, Weege B, Yan K, Edgar JM, Yagen- sky O, Wichert SP, Agarwal A, Karram K, Renier N, Tessier-Lavigne M, Rossner MJ, Káradóttir RT, Nave KA (2016) A neuronal PI(3,4,5)P3-dependent program of oligodendrocyte precursor recruitment and myelination. Nat Neurosci. 20: 10-15
  • Quintes S, Brinkmann BG, Ebert M, Fröb F, Kungl T, Arlt FA, Tarabykin V, Huylebroeck D, Meijer D, Suter U, Wegner M, Sereda MW, Nave KA (2016) Zeb2 is essential for Schwann cell differentiation, myelination and nerve repair. Nat Neurosci. 19: 1050-91
  • Fünfschilling U, Supplie LM, Mahad D, Boretius S, Saab AS, Edgar J, Brinkmann BG, Kassmann CM, Tzvetanova ID, Möbius W, Diaz F, Meijer D, Suter U, Hamprecht B, Sereda MW, Moraes CT, Frahm J, Goebbels S, Nave KA (2012). Glycolytic oligodendrocytes maintain myelin and long-term axonal integrity. Nature 485: 517-521
  • Nave K-A (2010) Myelination and support of axonal integrity by glia. Nature 468, 244-252