Download Frauke Zipp's Curriculum Vitae (Pdf , 121,4 KB)
After studying medicine in Germany, the USA, Canada and England, and three years of clinical neurology with a focus on neurodegenerative disorders, Frauke Zipp began her career at the Max Planck Institute Martinsried with Hartmut Wekerle where she investigated neuroimmunological aspects of multiple sclerosis. During further clinical training with Johannes Dichgans in Tübingen, she spent time as a visiting scientist at the National Institutes of Health. In the subsequent decade at the Charité, Frauke Zipp became professor in the Neurology Department and acted as the spokesperson of a Collaborative Research Center as well as a Training School, and ultimately as a Board Director of the Excellence Cluster “NeuroCure”. Thereafter, she moved to the Rhine-Main Neuroscience Network (rmn2) as the Director of the Department of Neurology at the University Medical Center Mainz within the Focus Program of Translational Neurosciences (FTN) and Immunotherapy (FZI). Frauke Zipp is member of the Gutenberg Research College, a strategic committee counseling the University President. Apart from participating on several advisory boards and reviewing for international journals, research agencies as well as research and clinical societies, Frauke Zipp has published in journals such as Nature Medicine, Lancet and Neuron. She is currently spokesperson of a Collaborative Research Center on Multiple Sclerosis, Executive Board Member of the Competence Network of Multiple Sclerosis (KKNMS), was a Council Member of ECTRIMS, is now Member of the Multiple Sclerosis International Federation (MSIF) and Board Member of the International Society of Neuroimmunology (ISNI) as well as was Conference President for the 12th ISNI Congress 2014. Frauke Zipp has performed several investigator initiated treatment trials. Her research focuses on the crosstalk of the immune and the nervous system in neuroimmunological diseases, T cell responses and immuneregulation in Multiple Sclerosis and inflammatory neuronal injury and repair.
Paterka M, Siffrin V, Voss JO, Werr J, Hoppmann N, Gollan R, Belikan P, Bruttger J, Birkenstock J, Esplugues E, Yogev N, Flavell RA, Bopp T, Zipp F. 2016. Gatekeeper role of antigen-presenting CD11c+ cells in neuroinflammation. EMBO Journal 35(1): 89-101.
Ulges A, Witsch E, Pramanik G, Klein M, Birkner K, Bühler U, Wasser, B, Luessi, F, Stergiou N, Dietzen S, Brühl T-J, Bohn T, Bündgen G, Kunz H, Waisman A, Schild H, Schmitt E, Zipp F§, Bopp T§. 2016. Protein kinase CK2 governs the molecular decision between encephalitogenic TH17 cell and Treg cell development. Proc Natl Acad Sci USA 113(36): 10145-50. § equally contributing
Larochelle C, Uphaus T, Prat A, Zipp F. 2016. Secondary progression in multiple sclerosis: neuronal exhaustion or distinct pathology? Trends Neurosci 39(5): 325-339
Ellwardt E, Walsh JT, Kipnis J, Zipp F. 2016. Understanding the Role of T Cells in CNS Homeostasis. Trends Immunol 37(2): 154-65.
Walsh, J. T., Hendrix, S., Boato, F., Smirnov, I., Zheng, J., Lukens, J. R., Gadani, S., Hechler, D., Golz, G., Rosenberger, K., Kammertons, T., Vogt, J., Vogelaar, C., Siffrin, V., Radjavi, A., Fernandez-Castaneda, A., Gaultier, A., Gold, R., Kanneganti, T. D., Nitsch, R., Zipp §, F., and Kipnis §, J. 2015. MHCII-independent CD4+ T cells protect injured CNS neurons via IL-4. J Clin Invest 125: 699-714. § equally contributing.
Methner, A., and Zipp, F. 2013. Multiple sclerosis in 2012: Novel therapeutic options and drug targets in MS. Nat Rev Neurol 9: 72-73.
Liblau, R. S., Gonzalez-Dunia, D., Wiendl, H., and Zipp, F. 2013. Neurons as targets for T cells in the nervous system. Trends Neurosci 36: 315-324.
IMSGC (Zipp F as part of strategy group). 2013. Analysis of immune-related loci identifies 48 new susceptibility variants for multiple sclerosis. Nat Genet 45: 1353-1360.
Roep, B. O., Buckner, J., Sawcer, S., Toes, R., and Zipp, F. 2012. The problems and promises of research into human immunology and autoimmune disease. Nat Med 18: 48-53.
IMSGC (Zipp F as part of strategy group). 2011. Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis. Nature 476: 214-219.
Siffrin, V., Vogt, J., Radbruch, H., Nitsch, R., and Zipp, F. 2010. Multiple sclerosis - candidate mechanisms underlying CNS atrophy. Trends Neurosci 33: 202-210.
Siffrin, V., Radbruch, H., Glumm, R., Niesner, R., Paterka, M., Herz, J., Leuenberger, T., Lehmann, S. M., Luenstedt, S., Rinnenthal, J. L., Laube, G., Luche, H., Lehnardt, S., Fehling, H. J., Griesbeck, O., and Zipp, F. 2010. In vivo imaging of partially reversible th17 cell-induced neuronal dysfunction in the course of encephalomyelitis. Immunity 33: 424-436.
Schulze-Topphoff, U., Prat, A., Prozorovski, T., Siffrin, V., Paterka, M., Herz, J., Bendix, I., Ifergan, I., Schadock, I., Mori, M. A., Van Horssen, J., Schroter, F., Smorodchenko, A., Han, M. H., Bader, M., Steinman, L., Aktas, O., and Zipp, F. 2009. Activation of kinin receptor B1 limits encephalitogenic T lymphocyte recruitment to the central nervous system. Nat Med 15: 788-793.
Prozorovski, T., Schulze-Topphoff, U., Glumm, R., Baumgart, J., Schroter, F., Ninnemann, O., Siegert, E., Bendix, I., Brustle, O., Nitsch, R., Zipp §, F., and Aktas §, O. 2008. Sirt1 contributes critically to the redox-dependent fate of neural progenitors. Nat Cell Biol 10: 385-394. § equally contributing.
Hoffmann, O., Priller, J., Prozorovski, T., Schulze-Topphoff, U., Baeva, N., Lunemann, J. D., Aktas, O., Mahrhofer, C., Stricker, S., Zipp §, F., and Weber §, J. R. 2007. TRAIL limits excessive host immune responses in bacterial meningitis. J Clin Invest 117: 2004-2013. § equally contributing.
Zipp, F., and Aktas, O. 2006. The brain as a target of inflammation: common pathways link inflammatory and neurodegenerative diseases. Trends Neurosci 29: 518-527.
Aktas, O., Smorodchenko, A., Brocke, S., Infante-Duarte, C., Schulze Topphoff, U., Vogt, J., Prozorovski, T., Meier, S., Osmanova, V., Pohl, E., Bechmann, I., Nitsch, R., and Zipp, F. 2005. Neuronal damage in autoimmune neuroinflammation mediated by the death ligand TRAIL. Neuron 46: 421-432.
Wandinger, K. P., Lunemann, J. D., Wengert, O., Bellmann-Strobl, J., Aktas, O., Weber, A., Grundstrom, E., Ehrlich, S., Wernecke, K. D., Volk, H. D., and Zipp, F. 2003. TNF-related apoptosis inducing ligand (TRAIL) as a potential response marker for interferon-beta treatment in multiple sclerosis. Lancet 361: 2036-2043.
Diestel, A., Aktas, O., Hackel, D., Hake, I., Meier, S., Raine, C. S., Nitsch §, R., Zipp §, F., and Ullrich §, O. 2003. Activation of microglial poly(ADP-ribose)-polymerase-1 by cholesterol breakdown products during neuroinflammation: a link between demyelination and neuronal damage. J Exp Med 198: 1729-1740. § equally contributing.
Aktas, O., Waiczies, S., Smorodchenko, A., Dorr, J., Seeger, B., Prozorovski, T., Sallach, S., Endres, M., Brocke, S., Nitsch, R., and Zipp, F. 2003. Treatment of relapsing paralysis in experimental encephalomyelitis by targeting Th1 cells through atorvastatin. J Exp Med 197: 725-733.
Nitsch, R., Bechmann, I., Deisz, R. A., Haas, D., Lehmann, T. N., Wendling, U., and Zipp, F. 2000. Human brain-cell death induced by tumour-necrosis-factor-related apoptosis-inducing ligand (TRAIL). Lancet 356: 827-828.
Zipp, F., Weil, J. G., and Einhaupl, K. M. 1999. No increase in demyelinating diseases after hepatitis B vaccination. Nat Med 5: 964-965.