Göttinger Graduiertenschule für Neurowissenschaften, Biophysik und Molekulare Biowissenschaften

Schulz, Jörg, Prof. Dr.

Professor of Restorative Neurobiology, Director of the Department of Neurodegeneration and Restorative Research
- MD, University of Cologne Medical School, 1991
- Training in Neurology and Neuroscience at the Department of Neurology in Tübingen
- DFG Research Fellow at the Massachusetts General Hospital and Harvard Medical School, Boston
- Head of Neurodegeneration Laboratory, Hertie Institute for Clinical Brain Research and University of Tübingen, 1998-2004
- Habilitation, University of Tübingen, 1999
- Director of the Department of Neurodegeneration and Restorative Research, CMPB, University of Göttingen, since 2004

Major Research Interests
Our Department studies the mechanisms of degeneration in neurodegenerative disorders, including Parkinson’s disease, Alzheimer’s disease and cerebral ataxias. Because increased age is the major risk factor for developing a neurodegenerative disorder, we are highly interested in the mechanisms of neuronal aging. To study these mechanisms we use immortalized cell line models, primary neuronal culture models, Drosophila models, toxin-induced and transgenic mammalian (mice, rats, primates) models of Parkinson’s disease. Once important pathogenetic steps have been identified we investigate their functional significance my using pharmacological or molecular tools including different transfection methods and viral gene transfer. The ultimate goal is to translate these findings into treatments that are applicable to patients. Therefore, the Department is enrolled in the outpatient clinics for Movemenet Disorders and Dementias and has a leading role in the German Network for Hereditary Movement Disorders (GeNeMove).

Homepage Department/Research Group:
http://www.neurodegeneration.uni-goettingen.de/

Selected Recent Publications
- Eberhardt O, von Coelln R, Kügler S, Lindenau J, Rathke-Hartlieb S, Gerhardt E, Haid S, Isenmann S, Gravel C, Srinivasan A, Bähr M, Weller M, Dichgans J, Schulz JB. Protection by synergistic effects of adenovirus-mediated X-chromosome-linked inhibitor of apoptosis and glial cell line-derived neurotrophic factor gene transfer in the 1-Methyl-4-Phenyl-1,2,3,6-tetrahydropyridine model of Parkinson’s disease. J. Neurosci. 2000, 20: 9126-9134.

- Xia XG, Harding T, Weller M, Uney JB, Schulz JB. Gene transfer of the JNK interacting protein-1 protects dopaminergic neurons in the MPTP model of Parkinson’s disease. Proc. Natl. Acad. Sci. USA, 2001, 98: 10433-10438.

- Wick A, Wick W, Waltenberger J, Weller M, Dichgans J, Schulz JB. Neuroprotection by hypoxic preconditioning requires sequential activation of vascular endothelial growth factor receptor and Akt. J. Neurosci. 2002, 22:6401-6407.

- Simons M, Krämer E-M, Macchi P, Rathke-Hartlieb S, Trotter J, Nave K-A, Schulz JB. Overexpression of the Myelin Proteolipid Protein leads to accumulation of cholesterol and Proteolipid Protein in endosomes/lysosomes: implications for Pelizaeus-Merzbacher disease. J. Cell Biol. 2002, 157: 327-336.

- Simons M, Schwärzler F, Lütjohann D, von Bergmann K, Beyreuther K, Dichgans J, Wormstall H, Hartmann T, Schulz JB. Treatment with simvastatin in normocholesterolemic patients with Alzheimer’s disease: a 26-week randomised, placebo-controlled, double-blind trial. Ann. Neurol. 2002, 52: 346-350.

- Luft AR, Buitrago MM, Ringer T, Dichgans J, Schulz JB. Motor skill learning depends on protein synthesis in motor cortex after training. J. Neurosci. 2004, 24: 6515-6520.

- Beier CP, Wischhusen J, Gleichmann M, Gerhardt E, Pekanovic A, Krueger A, Taylor V, Suter U, Krammer PH, Endres M, Weller M, Schulz JB. FasL (CD95L/APO-1L) resistance of neurons mediated by phosphatidylinositol 3-kinase-Akt/protein kinase B-dependent expression of lifeguard/neuronal membrane protein 35. J. Neurosci. 2005, 25: 6765-6774.

- Strauss K, Martins L.M., Plun-Favreau H, Marx F, Kautzmann S, Berg D, Gasser T, Wszolek Z, Müller T, Bornemann A, Wolburg H, Downward J, Riess O, Schulz JB, Krüger R. Loss of function mutations in the gene encoding Omi/HtrA2 in Parkinson’s disease. Hum. Mol. Genet. 2005, 14: 2099-2111.