Background: In Alzheimer's disease β-amyloid plaque deposits are accompanied by an inflammatory reaction involving microglia, which are the primary phagocytotic immune cells of the brain. Microglia cells are attracted to and surround amyloid plaques, suggesting a role in plaque formation and/or restricting unlimited plaque growth. Methods: Amyloid precursor protein transgenic mouse models (APPPS1 and APP23) have been crossed with CD11b-HSVTK transgenic mice. Results: These mice allow 30% and >90% microglia depletion upon systemic and intracerebroventricular ganciclovir application, respectively, for up to 4 weeks. Conclusions: Opposite to expectations, results show that amyloid plaque formation can occur in the absence of microglia and that microglia depletion in amyloid-bearing mice does not influence amyloid plaque load.
1Hertie-Institute for Clin. Brain Research, Tuebingen, Germany
2Institute for Neuropathology, Charité – Universitätsmedizin Berlin, Berlin, Germany
3Departments of Pathology and Psychiatry, New York University School of Medicine, New York, NY, USA
4Department of Radiation Oncology, University of Tuebingen, Tuebingen, Germany
5Department of Pathology, University of Tuebingen, Tuebingen, Germany
6Department of Neurochemistry, National Institute of Neuroscience, Tokyo, Japan