Prof. Dr. med. Ingo Bechmann
Microglia is the innate immune cell of the central nervous system and contributes to plasticity and learning e.g. by the removal of presynaptic buttons. They microglial population is substituted only upon massive neuropathological damage and thus, is re-populated only by mitosis of those cells, which arrived early in ontogeny. Consequently, if we turn 100 years, our microglia has the same age and exhibits signs of senescence in many humans. In human brains, we found that microglial senescence precedes the onset of neurodegeneration in Alzheimer’s disease (AD). As some genetic risk factors of AD are linked to phagocytosis, we hypothesize that microglial senescence leads to failure of the phagocytic capacity of microglia causing the accumulation of amyloid into amyloid plaques, a hallmark of AD, but also of other toxins yet to be discovered.
Major aims of our group are
- Identification of factors accumulating in the aging brain and driving microglial aging
- Understanding the role of microglia in AD
- Understanding how toxins are eliminated in the brain which lacks a lymphatic drainage system
Menzel F, Kaiser N, Haehnel S, Rapp F, Patties I, Schöneberg N, Haimon Z, Immig K, Bechmann I (2018). Impact of X-irradiation on microglia. Glia. 2018 Jan;66(1):15-33.
Engelhardt B, Carare RO, Bechmann I, Flügel A, Laman JD, Weller RO (2016). Vascular, glial, and lymphatic immune gateways of the central nervous system. Acta Neuropathol. 2016 Sep;132(3):317-38.
Tischer J, Krueger M, Mueller W, Staszewski O, Prinz M, Streit WJ, Bechmann I (2016). Inhomogeneous distribution of Iba-1 characterizes microglial pathology in Alzheimer's disease. Glia. 2016 Sep; 64(9): 1562-72.
Goldmann T, Wieghofer P, Jordão MJ, Prutek F, Hagemeyer N, Frenzel K, Amann L, Staszewski O, Kierdorf K, Krueger M, Locatelli G, Hochgerner H, Zeiser R, Epelman S, Geissmann F, Priller J, Rossi FM, Bechmann I, Kerschensteiner M, Linnarsson S, Jung S, Prinz M. Origin (2016). Fate and dynamics of macrophages at central nervous system interfaces. Nat Immunol. 2016 Jul;17(7):797-805.
Immig K, Gericke M, Menzel F, Merz F, Krueger M, Schiefenhövel F, Lösche A, Jäger K, Hanisch UK, Biber K, Bechmann I (2015). CD11c-positive cells from brain, spleen, lung, and liver exhibit site-specific immune phenotypes and plastically adapt to new environments. Glia. 2015 Apr;63(4):611-25.
Streit WJ, Xue QS, Tischer J, Bechmann I (2014). Microglial pathology. Acta Neuropathol Commun. 2014 Sep 26;2:142.
Prodinger C, Bunse J, Krüger M, Schiefenhövel F, Brandt C, Laman JD, Greter M, Immig K, Heppner F, Becher B, Bechmann I (2011). CD11c-expressing cells reside in the juxtavascular parenchyma and extend processes into the glia limitans of the mouse nervous system. Acta Neuropathol. 2011 Apr; 121(4): 445-58.
Streit WJ, Braak H, Xue QS, Bechmann I (2009). Dystrophic (senescent) rather than activated microglial cells are associated with tau pathology and likely precede neurodegeneration in Alzheimer's disease. Acta Neuropathol. 2009 Oct;118(4):475-85.
Frank S, Burbach GJ, Bonin M, Walter M, Streit W, Bechmann I, Deller T (2008). TREM2 is upregulated in amyloid plaque-associated microglia in aged APP23 transgenic mice. Glia. 2008 Oct;56(13):1438-47.
Bechmann I, Galea I, Perry VH (2007). What is the blood-brain barrier (not)? Trends Immunol. 2007 Jan;28(1):5-11.
Kwidzinski E, Bunse J, Aktas O, Richter D, Mutlu L, Zipp F, Nitsch R, Bechmann I (2005). Indolamine 2,3-dioxygenase is expressed in the CNS and down-regulates autoimmune inflammation. FASEB J. 2005 Aug;19(10):1347-9.
Bechmann I, Goldmann J, Kovac AD, Kwidzinski E, Simbürger E, Naftolin F, Dirnagl U, Nitsch R, Priller J (2005). Circulating monocytic cells infiltrate layers of anterograde axonal degeneration where they transform into microglia. FASEB J. 2005 Apr;19(6):647-9.