Bähr, Mathias, Prof. Dr.
Professor of Neurology
- 1985 MD, University of Tübingen Medical School, Training in Neurology at University Hospitals in Tübingen and Düsseldorf
- DFG and Max Planck Fellow at the Max Planck Institute for Developmental Biology Tübingen and at the Department of Anatomy and Cell Biology, Washington University St.Louis
- Schilling Foundation Professor for Clinical and Experimental Neurology, University of Tübingen
- Since 2001 Director of the Department of Neurology, University of Göttingen
Major Research Interests
Neuronal cell loss is not only a major feature of human neurodegenerative diseases like Parkinson?s disease (PD), Alzheimer?s disease (AD) or stroke, but can also be observed in neuroinflammatory conditions like Multiple Sclerosis (MS) or after traumatic lesions. We examine the cellular and molecular mechanisms of neuronal dysfunction and neuronal cell death in
animal models of the respective disorders with the ultimate goal to detect new targets for a therapeutic neuroprotective intervention.
We have used for many years the retino-tectal system in rodents as our standard model to study de-and regeneration in vitro and in vivo. Our group has in detail analysed the cellular and molecular cascades that follow lesions of the optic nerve and ultimately lead to cell death of the retinal ganglion cells. To monitor the changes that occur directly after lesions we succeeded in implementing in vivo life-imaging of the rat and mouse optic nerve, which offers us a unique opportunity to study the complex processes that follow traumatic or inflammatory lesions of CNS fibre tracts.
In classical neurodegeneration research we have choosen PD as our topic. In this field, a multidisciplinary research team with our participation in the area C2 of the excellence cluster CNMPB examines the role of a-synuclein aggregation for dopaminergic dysfunction and cell death and characterizes other disease related proteins in order to develop new neuroprotective strategies.
In all our model systems we use AAV-mediated viral gene transfer to express different disease-or de-/regeneration associated genes as research tools and also as potential therapeutic factors to manipulate the respective molecular events in vitro and in vivo. To that end, we have e.g. developed regulatory elements that allow a controlled gene expression in complex in vivo models.
The final aim of our research approaches is to describe in detail the molecular pathophysiology that leads to axonal and neuronal loss and to develop new therapeutic strategies, some of which have already been translated into proof of concept studies in human patients.
Homepage Department/Research Group
Selected Recent Publications
- J.Knöferle, J.C. Koch, T. Ostendorf, U.Michel, V.Planchamp, P.Vutova, L.Tönges, C.Stadelmann, W.Brück, M.Bähr and P.Lingor (2010) Mechanisms of acute axonal degeneration in the optic nerve in vivo. Proc Natl Acad Sci U S A. 107(13):6064-9.
- Koch JC, Knöferle J, Tönges L, Michel U, Bähr M, Lingor P. (2011) Imaging of rat optic nerve axons in vivo. Nat Protoc. 3;6(12):1887-96.
- Doeppner TR, Kaltwasser B, Fengyan J, Hermann DM, Bähr M. (2013) TAT-Hsp70 induces neuroprotection against stroke via anti-inflammatory actions providing appropriate cellular microenvironment for transplantation of neural precursor cells. J Cereb Blood Flow Metab. 33(11):1778-88.
- Kretzschmar B, Hein K, Moinfar Z, Könnecke B, Sättler MB, Hess H, Weissert R, Bähr M. (2014) Treatment with atacicept enhances neuronal cell death in a rat model of optic neuritis. J Neuroimmunol. Mar 15;268(1-2):58-63.
- Eckermann K, Kügler S, Bähr M. (2015) Dimerization propensities of Synucleins are not predictive for Synuclein aggregation. Biochim Biophys Acta. 1852(8):1658-64
- Ribas VT, Schnepf B, Challagundla M, Koch JC, Bähr M, Lingor P. (2015) Early and sustained activation of autophagy in degenerating axons after spinal cord injury. Brain Pathol. 25(2):157-70
- Tereshchenko J, Maddalena A, Bähr M, Kügler S. (2014) Pharmacologically controlled, discontinuous GDNF gene therapy restores motor function in a rat model of Parkinson's disease. Neurobiol Dis. 65:35-42