Dr. Martin Fuhrmann
Group Leader
German Center for Neurodegenerative Diseases (DZNE)
BMZ 1 - Building 344
Sigmund-Freud-Str. 25
53105 Bonn
martin.fuhrmann(at)dzne.de
+49 (0) 228 / 287-52173
+49 (0) 228 / 287-51619
More information
Areas of investigation/research focus
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 cell, 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 at 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 synapse and neuron loss under neurodegenerative conditions. Standard molecular biological, biochemical and immunohistochemical techniques complement our state of the art in vivo multiphoton imaging expertise.
Publications
Role of presenilin1 in structural plasticity of cortical dendritic spines in vivo.
CK Jung, M Fuhrmann, K Honarnejad, F Van Leuven, J Herms; J Neurochem. 2011 Dec;119(5):1064-73. doi: 10.1111/j.1471-4159.2011.07503.x. Epub 2011 Oct 24.
In vivo multiphoton imaging reveals gradualgrowth of newborn amyloid plaques over weeks.
Burgold S, Bittner T, Dorostkar MM, Kieser D, Fuhrmann M, Mitteregger G, Kretzschmar H, Schmidt B, Herms J. Acta Neuropathol. 2010 Dec 7. [Epub ahead of print] PubMed PMID: 21136067.
Multiple events lead to dendritic spine loss in triple transgenic Alzheimer's disease mice.
Bittner T, Fuhrmann M, Burgold S, Ochs SM, Hoffmann N, Mitteregger G, Kretzschmar H, Laferla FM, Herms J, PLoS One. 2010 Nov 16;5(11):e15477. PubMed PMID: 21103384.
Microglial Cx3cr1 knockout prevents neuron loss in a mouse model of Alzheimer's disease.
Fuhrmann M, Bittner T, Jung CK, Burgold S, Page RM, Mitteregger G, Haass C, LaFerla FM, Kretzschmar H, Herms J, Nat Neurosci. 2010 Apr;13(4):411-3. Epub 2010 Mar 21. PubMed PMID: 20305648.
Real-time imaging reveals the single steps of brain metastasis formation.
Kienast Y, von Baumgarten L, Fuhrmann M, Klinkert WE, Goldbrunner R, Herms J, Winkler F, Nat Med. 2010 Jan;16(1):116-22. Epub 2009 Dec 20. PubMed PMID: 20023634.
Gamma-secretase inhibition reduces spine density in vivo via an amyloid precursor protein-dependent pathway.
Bittner T, Fuhrmann M, Burgold S, Jung CK, Volbracht C, Steiner H, Mitteregger G, Kretzschmar HA, Haass C, Herms J, J Neurosci. 2009 Aug 19;29(33):10405-9. PubMed PMID: 19692615.
Imaging glioma cell invasion in vivo reveals mechanisms of dissemination and peritumoral angiogenesis.
Winkler F, Kienast Y, Fuhrmann M, Von Baumgarten L, Burgold S, Mitteregger G, Kretzschmar H, Herms J, Glia. 2009 Sep;57(12):1306-15. PubMed PMID: 19191326.
Tumor-selective vessel occlusions by platelets after vascular targeting chemotherapy using paclitaxel encapsulated in cationic liposomes.
Strieth S, Nussbaum CF, Eichhorn ME, Fuhrmann M, Teifel M, Michaelis U, Berghaus A, Dellian M, Int J Cancer. 2008 Jan 15;122(2):452-60. PubMed PMID: 17918179.
Dendritic pathology in prion disease starts at the synaptic spine.
Fuhrmann M, Mitteregger G, Kretzschmar H, Herms J, J Neurosci. 2007 Jun 6;27(23):6224-33. PubMed PMID: 17553995.
Loss of the cellular prion protein affects the Ca2+ homeostasis in hippocampal CA1 neurons.
Fuhrmann M, Bittner T, Mitteregger G, Haider N, Moosmang S, Kretzschmar H, Herms J, J Neurochem. 2006 Sep;98(6):1876-85. PubMed PMID: 16945105.
Cortical dysplasia resembling human type 2 lissencephaly in mice lacking all three APP family members.
Herms J, Anliker B, Heber S, Ring S, Fuhrmann M, Kretzschmar H, Sisodia S, Müller U, EMBO J. 2004 Oct 13;23(20):4106-15. Epub 2004 Sep 23. PubMed PMID: 15385965; PubMed Central PMCID: PMC524337.


