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Mathias Bähr

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
Director at the Department of Neurology, University of Göttingen since 2001

Major Research Interests:

Mathias Bähr

We are interested to understand 2 basic questions in cellular and molecular neurobiology:

1. Which factors support survival of adult CNS neurons?

2. What kills these cells under pathological conditions?

Up to now, only little is known about the mechanisms that support survival of a postmitotic cell like a human neuron for eventually more than 100 years under physiological conditions. However, by examining the molecular regulation of cell survival and cell death during development and in the lesioned adult CNS, one may get some clues to answer this question.

In our group, several in vitro and in vivo model systems are used which allow examination of neuronal de- and regeneration. Our basic model is the rodent retino-tectal projection. Here, we can study development, de- and regeneration of the respective projection neurons, the retinal ganglion cells (RGCs) in single cell cultures, explants or in vivo. Transection or crush-axotomy of the optic nerve induces retrograde death more than 80% of RGCs within two weeks. This secondary cell loss is mainly apoptotic and involves specific changes in gene expression pattern of transcription factors (e.g. c-jun or ATF-2), pro- and anti-apoptotic genes (e.g. bcl-2 or bax) and growth-associated genes (like GAP-43). Thus, long term survival and initiation of regeneration programmes of RGCs critically depends on inhibition of apoptotic cell death. To that end, we have used a variety of techniques to interfere with the cell death cascades that follow lesions of the optic nerve in adult rats. Inhibition of neuronal apoptosis can be afforded by pharmacological administration of trophic factors or by gene therapy approaches using adenovirus vectors that can deliver neurotrophic factors directly into neurons or into surrounding glial cells. These, an other new strategies like using transduction-domains to deliver anti-apoptotic proteins across the blood-brain-barrier are now used to develop new experimental therapy strategies in animal models of human neurological disorders like stroke, trauma, multiple sclerosis od neurodegenerative diseases (e.g. Alzheimer ´s or Parkinson´s disease).

Zentrum Neurologische
Medizin, Neurologie
Universität Göttingen
Robert-Koch-Str. 40

37075 Göttingen

phone:+49-551-39 6603
fax:+49-551-39 8405

Further Information:

Selected Recent Publications:

Klöcker N, Kermer P, Weishaupt JH, Labes M, Ankerhold R, Bähr M (2000) BDNF mediated neuroprotection of adult rat retinal ganglion cells in vivo does not exclusively depend on PI-3-K/PKB signalling. J Neurosci 20: 6962-6967

Bähr M (2000) Live and let die - Survival and cell death in the developing and lesioned adult CNS. TINS 23(10): 483-490

Diem R, Meyer R, Weisshaupt J, Bähr M (2001) Reduction of potassium currents and PI3-K-dependent Akt phosphorylation by tumor necrosis factor a rescues axotomized retinal ganglion cells from secondary cell death in vivo . J Neurosci 21(6): 2058-2066

Meyer R, Weissert R, Graaf K de, Diem R, Bähr M (2001) Acute neuronal apoptosis in a rat model of multiple sclerosis. J Neurosci 21: 6214-6220

Kilic E, Dietz GPH, Herrmann DM, Bähr M (2002) Intravenous TAT-Bcl-XL is protective when delivered before and after middle cerebral artery occlusion in mice. Ann Neurol: in press