Research group leader
Neuroimmunology & Imaging
German Center for Neurodegenerative Diseases (DZNE), Bonn
c/o Biomedizinisches Zentrum Geb. 344
D- 53127 Bonn
Phone +49 (0) 228 287-52173
Curriculum vitae Dr. Martin Fuhrmann
The brain consists of a huge number of neurons. The often neglected glial cells are equally abundant or may even outnumber neurons in brain tissue. Specialized glial cells, the microglia, represent the immune system in the brain. Historically, microglia were believed to be sessile cells staying in a resting state becoming activated under inflammatory conditions. This opinion changed with the finding that microglia actively screen the surrounding brain parenchyma by constantly protracting and retracting their filopodial fine processes on the minute time-scale. We are interested in the communication of glia and neurons under neurodegenerative conditions like Alzheimer’s disease. Therefore, we use in vivo two-photon imaging over time periods of months to analyze structural and functional changes during disease progression. We analyze neuro-glia communication signals on the molecular level utilizing transgenic and knockout mouse models in combination with neurodegenerative disease mouse models. Additionally, we are interested in basic mechanisms underlying synapses and neuron loss under neurodegenerative conditions.
Two-photon in vivo imaging; Optogenetics; mouse models; immunohistochemistry.
5 most important publications
1. Fuhrmann M, Bittner T, Jung CK, Burgold S, Page RM, Mitteregger G, Haass C, LaFerla FM, Kretzschmar H, Herms J. (2010) Microglial Cx3cr1 knockout prevents neuron loss in a mouse model of Alzheimer’s disease. Nat Neurosci, 13(4): 411-413.
2. Kienast Y, von Baumgarten L, Fuhrmann M, Klinkert WE, Goldbrunner R, Herms J, Winkler F. (2010) Real-time imaging reveals the single steps of brain metastasis formation. Nat Med, 16(1): 116-122.
3. Bittner T, *Fuhrmann M, Burgold S, Ochs SM, Hoffmann N, Mitteregger G, Kretzschmar H, LaFerla FM, Herms J. (2010) Multiple events lead to dendritic spine loss in triple transgenic Alzheimer’s disease mice. PLoS One, 5(11): e15477. (*equal contribution).
4. Bittner T, Fuhrmann M, Burgold S, Jung CK, Volbracht C, Steiner H, Mitteregger G, Kretzschmar HA, Haass C, Herms J. (2009) Gamma-secretase inhibition reduces spine density in vivo via an amyloid precursor protein-dependent pathway. J Neurosci, 29(33): 10405-10409.
5. Fuhrmann M, Mitteregger G, Kretzschmar H, Herms J. (2007) Dendritic pathology in prion disease starts at the synaptic spine. J Neurosci, 27(23): 6224-6233.