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Formation and maintenance of Alzheimer's disease bold beta-amyloid plaques in the absence of microglia

in
Publisher: 
Nature Neuroscience
Author: 
Stefan A Grathwohl1,2,3,12, Roland E Kälin4,12, Tristan Bolmont1,2, Stefan Prokop4, Georg Winkelmann4, Stephan A Kaeser1,2, Jörg Odenthal1,2, Rebecca Radde1,2, Therese Eldh5, Sam Gandy6, Adriano Aguzzi7, Matthias Staufenbiel8, Paul M Mathews9,10, Hartwig Wolburg11, Frank L Heppner4,13 & Mathias Jucker1,2,13
Date published: 
18 October, 2009
Region: 
International

Publication type: 
research
Publication link: 
Formation and maintenance of Alzheimer's disease bold beta-amyloid plaques in the absence of microglia
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In Alzheimer's disease, microglia cluster around beta-amyloid deposits, suggesting that these cells are important for amyloid plaque formation, maintenance and/or clearance. We crossed two distinct APP transgenic mouse strains with CD11b-HSVTK mice, in which nearly complete ablation of microglia was achieved for up to 4 weeks after ganciclovir application. Neither amyloid plaque formation and maintenance nor amyloid-associated neuritic dystrophy depended on the presence of microglia.

  1. Department of Cellular Neurology, Hertie-Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany.
  2. German Center for Neurodegenerative Diseases, Tübingen, Germany.
  3. Graduate School of Cellular and Molecular Neuroscience, University of Tübingen, Tübingen, Germany.
  4. Department of Neuropathology, Charité–Universitätsmedizin Berlin, Berlin, Germany.
  5. Department of Radiation Oncology, University of Tübingen, Tübingen, Germany.
  6. Department of Neurology, Mount Sinai School of Medicine, New York, New York, USA.
  7. Institute of Neuropathology, Department of Pathology, University Hospital, Zürich, Switzerland.
  8. Novartis Institutes for Biomedical Research, Nervous System Research, Basel, Switzerland.
  9. Nathan Kline Institute, Orangeburg, New York, USA.
  10. Departments of Psychiatry, New York University School of Medicine, New York, New York, USA.
  11. Department of Pathology, University of Tübingen, Tübingen, Germany.
  12. These authors contributed equally to this work.
  13. These authors jointly directed the study.

Correspondence to: Frank L Heppner4,13 e-mail: frank.heppner@charite.de

Correspondence to: Mathias Jucker1,2,13 e-mail: mathias.jucker@uni-tuebingen.de

 

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