Short CV
From 1991 Thomas Misgeld studied medicine at Technische Universität München. From 1993 to 1999 he performed research with Prof. H. Wekerle for his M.D. thesis at the Max-Planck-Institute of Neurobiology (department of Neuroimmunology) in Martinsried. For his efforts he received the thesis award for the best thesis in medicine from TUM. In 1999 he was awarded his Ph.D. degree at TUM and started an internship at the Institute of Clinical Neuroimmunology at Ludwig-Maximilians-University in Munich. From 2000 to 2004 he worked with Prof. J. Lichtman as Post-doctoral fellow at the Department of Anatomy and Neurobiology at Washington University in St. Louis (USA). In 2004 Misgeld joined Harvard University in Cambridge as a Post-doctoral fellow at the Department of Molecular and Cellular Biology. Since September 2006 he runs his own laboratory, which is located at the TUM Institute of Neuroscience. Presently Misgeld is a W3-Professor for Biomolecular Sensors at TUM and the Center for Integrated Protein Science (CIPSM).
Selected Awards
- 2007, Schilling-Award, German Neuroscience Society
- 2006, Sofja-Kovalevskaja Award, Alexander-of-Humboldt Foundation
- 2005, Robert-Feulgen Award, Histochemical Society
- 2004, Wyeth young investigator Prize in multiple sclerosis
Research Interests
The Misgeld lab studies axon changes in the healthy and in the sick nervous system of living animals. Axons are the long neuronal processes that form synapses and thus interconnect different parts of the nervous system.
Obviously, to properly establish wiring in the brain, myriads of axons have to find their targets, or otherwise, axons that connect incorrectly need to be removed. We are interested in the latter process - not only because such axon dismantling contributes fundamentally to brain development and to the adaptation of neural circuits to the environment, but also because axons are highly susceptible to pathology. Many common neurological diseases are characterized by early loss of axonal connections - including motor neuron disease, spinal cord injury and multiple sclerosis, all of which we study.
By better understanding axon dismantling in development and disease we hope to gain insight into what causes axons to disintegrate in disease.
Selected Publications
- Misgeld, Thomas; Kerschensteiner, Martin: In vivo imaging of the diseased nervous system. Nature Reviews Neuroscience 7 (6), 2006, 449-463.
- Bareyre, Florence M; Kerschensteiner, Martin; Misgeld, Thomas; Sanes, Joshua R: Transgenic labeling of the corticospinal tract for monitoring axonal responses to spinal cord injury. Nature Medicine 11 (12), 2005, 1355-1360.
- Kerschensteiner, Martin; Schwab, Martin E; Lichtman, Jeff W; Misgeld, Thomas: In vivo imaging of axonal degeneration and regeneration in the injured spinal cord. Nature Medicine 11 (5), 2005, 572-577.
- Bishop, Derron L.; Misgeld, Thomas; Walsh, Mark K.; Gan, Wen-Biao; Lichtman, Jeff W.: Axon Branch Removal at Developing Synapses by Axosome Shedding. Neuron 44 (4), 2004, 651-661.
- Bidoia, C.; Misgeld, T.; Weinzierl, E.; Buffelli, M.; Feng, G.; Cangiano, A.; Lichtman, J.W.; Sanes, J.R.: Comment on "Reelin Promotes Peripheral Synapse Elimination and Maturation". Science 303 (5666), 2004, 1977b-1977b.
- Misgeld, Thomas; Burgess, Robert W; Lewis, Renate M; Cunningham, Jeanette M; Lichtman, Jeff W; Sanes, Joshua R: Roles of Neurotransmitter in Synapse Formation. Neuron 36 (4), 2002, 635-648.
Publications as TUM-IAS-Fellow