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New PET imaging biomarker could better predict progression of Alzheimer's disease

Press releases may be edited for formatting or style | April 05, 2019 Alzheimers/Neurology Molecular Imaging

"This study provides the first evidence that the level of microglial activation could be a far better predictor of current and future cognitive performance than beta-amyloid levels," noted Brendel. "Keeping the limitations of mouse models in mind, it could be crucial to modify an individual's microglial activation state to ameliorate future cognitive decline. We believe that a balanced microglia activation is crucial for prevention of cognitive impairment."

The authors of "Early and Longitudinal Microglial Activation but Not Amyloid Accumulation Predicts Cognitive Outcome in PS2APP Mice" include Carola Focke, Maximilian Deussing, Claudio Schmidt, Simon Lindner, Franz-Josef Gildehaus, Leonie Beyer and Barbara von Ungern-Sternberg, Department of Nuclear Medicine, University Hospital of Munich, LMU Munich, Munich, Germany; Tanja Blume, Department of Nuclear Medicine, University Hospital of Munich, LMU Munich, Munich, Germany, and Center for Neuropathology and Prion Research, Ludwig-Maximilians-University of Munich, Munich, Germany; Benedikt Zott and Helmuth Adelsberger, Institute of Neuroscience, Technical University of Munich, Munich, Germany; Yuan Shi and Mario M. Dorostkar, Center for Neuropathology and Prion Research, Ludwig-Miximilians-University of Munich, Munich, Germany, and DZNE-German Center for Neurodegenerative Diseases, Munich, Germany; Finn Peters, DZNE-German Center for Neurodegenerative Diseases, Munich, Germany; Gernot Kleinberger, Munich Cluster for Systems Neurology, University of Munich, Munich, Germany, and Biomedical Center, Biochemistry, Ludwig-Maximilians-University of Munich, Munich, Germany; Peter Bartenstein and Matthias Brendel, Department of Nuclear Medicine, University Hospital of Munich, LMU Munich, Munich, Germany, and Munich Cluster for Systems Neurology, University of Munich, Munich, Germany; Laurence Ozmen and Karlheinz Baumann, Roche Pharma Research and Early Development, F. Hoffman-La Roche Ltd., Basel, Switzerland; Christian Haass, DZNE-German Center for Neurodegenerative Diseases, Munich, Germany, Munich Cluster for Systems Neurology, University of Munich, Munich, Germany, and Biomedical Center, Biochemistry, Ludwig-Maximilians-University of Munich, Munich, Germany; Jochen Herms, Center for Neuropathology and Prion Research, Ludwig-Maximilians-University of Munich, Munich, Germany, DZNE-German Center for Neurodegenerative Diseases, Munich, Germany, and Munich Cluster for Systems Neurology, University of Munich, Munich, Germany; Axel Rominger, Department of Nuclear Medicine, University Hospital of Munich, LMU Munich, Munich, Germany, Munich Cluster for Systems Neurology, University of Munich, Munich, Germany, and Department of Nuclear Medicine, Inselspital, University Hospital Bern, Bern, Switzerland.

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