Microglia and Neuroinflammation
Dr. Annett Halle
Group Leader
Sigmund-Freud-Str. 27
53127 Bonn

annett.halle@dzne.de
 +49 228 43302-475

Areas of investigation/research focus

Microglial cells are cells of the innate immune system in the brain and act as the first form of immune defense in the central nervous system. Furthermore, microglial cells are key players in brain maintenance by constantly interacting with neurons and synapses and acting as scavenger cells.

Microglial cells play an important role in the initiation and progression of Alzheimer’s disease.

We are interested in the molecular mechanisms that shape microglial behavior under physiological conditions and in Alzheimer’s disease.

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We address questions such as: How do microglial properties, such as their phagocytic capacity or cell motility, change during Alzheimer’s disease? Do these changes influence disease progression? Are microglial changes dependent on the disease stage? Is there one homogeneous population of microglial cells in the Alzheimer’s brain or are there functional subgroups? Which signaling pathways are activated in Alzheimer’s disease and can they be modulated in a therapeutically meaningful way?

To address these open issues, we use cell biological and functional assays and work in close collaboration with DZNE-based groups on the transcriptomic regulation in microglia. Furthermore, we have developed innovative microscopy-based techniques and image analysis software to study the cellular behavior of microglia in cell culture and in animal models of Alzheimer’s disease.

Key Publications

Plescher M, Seifert G, Hansen JN, Bedner P, Steinhäuser C, Halle A. Plaque-dependent morphological and electrophysiological heterogeneity of microglia in an Alzheimer's disease mouse model. Glia. 2018 Mar 01; [Epub ahead of print] doi: 10.1002/glia.23318
Krabbe G*, Halle A*, Matyash V, Rinnenthal JL, Eom GD, Bernhardt U, et al. Functional impairment of microglia coincides with Beta-amyloid deposition in mice with Alzheimer-like pathology. PloS one. 2013 Jan 01; 8:e60921. doi: 10.1371/journal.pone.0060921
Hornung V, Bauernfeind F, Halle A, Samstad EO, Kono H, Rock KL, et al. Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization. Nat Immunol. 2008 Jan 01; 9:847-56. doi: 10.1038/ni.1631
Halle A, Hornung V, Petzold GC, Stewart CR, Monks BG, Reinheckel T, et al. The NALP3 inflammasome is involved in the innate immune response to amyloid-beta. Nat Immunol. 2008 Jan 01; 9:857-65. doi: 10.1038/ni.1636
Bermpohl D*, Halle A*, Freyer D, Dagand E, Braun JS, Bechmann I, et al. Bacterial programmed cell death of cerebral endothelial cells involves dual death pathways. J Clin Invest. 2005 Jan 01; 115:1607-15. doi: 10.1172/jci23223

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