Martin Kerschensteiner
Martin Kerschensteiner studied medicine at the University of Aachen and performed his MD thesis at the Department of Neuroimmunology of the Max-Planck-Institute of Neurobiology in Martinsried. He obtained his MD in 2000. After completing his postdoctoral training at the University and ETH Zurich, from 2001 to 2003, he worked as a research associate at Washington University (St Louis, USA) and Harvard University (Cambridge, USA) from 2003 to 2005. He then established his laboratory as an Emmy Noether research fellow of the German Research Foundation (DFG) at the Medical Center of the Ludwig-Maximilians-University Munich. He became associate professor for translational neuroimmunology in 2008, and is, since 2013, full professor and director of the Institute of Clinical Neuroimmunology at the Ludwig Maximilians University in Munich. His laboratory focuses on understanding how immune cells damage the nervous system, how reciprocal interactions between immune and nervous system control the formation and resolution of such inflammatory reactions. Within the FOR 5705 he wants to understand how neurons shape macrophage actions during autoimmune CNS inflammation.
Publications
A genome-wide in vivo CRISPR screen identifies essential regulators of T cell migration to the CNS in a multiple sclerosis model. Kendirli A., de la Rosa C., Lämmle K.F. et al. Nat Neurosci. 26, 1713-1725 (2023).
Targeting the TCA cycle can ameliorate widespread axonal energy deficiency in neuroinflammatory lesions. Tai Y.H., Engels D., Locatelli G. et al. Nat Metab. 5, 1364-1381 (2023).
Remyelination by surviving oligodendrocytes is inefficient in the inflamed mammalian cortex. Mezydlo A., Treiber N., Ullrich Gavilanes E.M. et al. Neuron. 111, 1748-1759.e8 (2023).
Phagocyte-mediated synapse removal in cortical neuroinflammation is promoted by local calcium accumulation. Jafari M., Schumacher A.M., Snaidero N. et al. Nat Neurosci. 24, 355-367 (2021).
Calcium Influx through Plasma-Membrane Nanoruptures Drives Axon Degeneration in a Model of Multiple Sclerosis. Witte M.E., Schumacher A.M., Mahler C.F. et al. Neuron. 101, 615-624.e5 (2019).
Links
Institute of Clinical Neuroimmunology
Institution
Munich