Dr. rer. nat. Anke Witting

Experimentelle Neurologie

AG Neuroinflammation

Position: Gruppenleiterin

Adresse: Helmholtzstrasse 8/1

89081 Ulm

Tel.: ++49-731-50063113


E-mail:            anke.witting@uni-ulm.de

webpage:       AG Witting

Kurz CV:

1991 – 1997    Studium der Biologie, Carl-von-Ossietzky Universität Oldenburg

1997 – 2000    Doktorarbeit, Max-Delbrück-Centrum (MDC) Berlin

11/2000           Promotion zum Dr.rer.nat., Humboldt Universität Berlin

2001 – 2005    Senior Fellow an der University of Washington, Department of Pharmacology,

                        Seattle, USA

2005 – 2006    Senior Fellow an der University of Washington, Department of Pathology, Seattle,


seit 2007  Gruppenleiterin, Universität Ulm

Kurzbeschreibung des Forschungsgebiets:

Neurodegenerative disorders, like Huntington’s disease (HD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS) and Alzheimer’s disease (AD) are not only characterized by neuronal death and loss of neuronal function but also by neuroinflammation. Microglia cells, the resident macrophages of the brain, play a central role in this neuroinflammation. The main functions of microglia are tissue maintenance and immune regulation. For this they are constantly surveying their environment. Almost any disturbance in the cellular environment will lead to microglia activation. Activated microglia are therefore a very early hallmark of neurodegenerative diseases. Furthermore this microglia activation often correlates with disease progression. Microglia activations might be beneficial and/or harmful for the surrounding neuronal tissue. For neurodegenerative diseases it is not yet known if the associated microglia activation is beneficial or harmful. Studies on ALS mice suggest that mutations that cause the disease and that are expressed by microglia cells induce a harmful microglia activation that speed disease progression. Targeting specifically this harmful microglia activation would be of great therapeutic value.

In addition to microglia activation neurodegenerative disorders are also characterized by mitochondrial dysfunction. In neurological disease like HD and PD as well as in aging the mitochondrial dysfunction is mediated by an inhibition of the transcriptional co-activator PGC-1 (PPAR  coactivator-1). PGC-1 belongs to the PGC-family of metabolic master regulators and induces the expression of mitochondrial proteins. PGC-family regulated genes very important for inflammatory responses, especially for a specific anti-inflammatory response of macrophages, the alternative activation or M2 activation. We have recently shown that mitochondrial function is essential for this alternative activation in microglia (Ferger et a., 2010).

Our group focuses on the mechanisms by which mutations that are linked to neurodegenerative diseases, especially to ALS and HD, modulate the activation of microglia. For this we focus on the link between mitochondrial dysfunction and inflammatory responses with regard to the PPAR and PGC-system. We hope to identify a mechanism in neurodegenerative diseases that links the mitochondrial dysfunction directly to the harmful microglia activation making this mechanism a valuable target for therapeutics.

Auswahl der wichtigsten Publikationen

Ferger A.I., Campanelli L., Reimer V., Muth K.N., Merdian I., Ludolph A.C. and Witting A. (2010) The effect of mitochondrial dysfunction on the immunological properties of microglia, J NEUROINFLAMMATION 7:45

Witting A., Chen L., Cudaback E., Straiker A., Walter L., Rickman B., Möller T., Brosnan C. and Stella N. (2006) Experimental autoimmune encephalomyelitis disrupts endocannabinoid-mediated neuroprotection. PNAS 103 (16): 6362-7

Eljaschewitsch E., Witting A., Mawrin C., Lee T., Schmidt P.M., Wolf S., Hoertnagl H., Raine C.S., Schneider-Stock R., Nitsch R. and Ullrich O. (2006) The endocannabinoid anandamide protects neurons during CNS inflammation by induction of MKP-1 in microglial cells. NEURON 49 (1): 67-79

Weydt P., Hong S.Y., Witting A., Moeller T., Stella N. and Kliot M. (2005) Cannabinol delays symptom onset in SOD1 (G93A) transgenic mice without affecting survival. AMYOTROPH LATERAL SCLER OTHER MOTOR NEURON DISORD 6 (3): 182-184

Witting A., Weydt P., Hong S.Y., Kliot M., Möller T. and Stella N. (2004) Endocannabinoids accumulate in spinal cord of SOD1 G93A transgenic mice.

J NEUROCHEM 89 (6): 1555-1557

Witting A., Walter L., Wacker J., Möller T. and Stella N. (2004) P2X7 receptors control 2-arachidonylglycerol production by microglial cells.

PNAS 101 (9): 3214-3219