Prion-like behaviour and tau-dependent cytotoxicity of pyroglutamylated amyloid-β

Justin M. Nussbaum, Stephan Schilling, Holger Cynis, Antonia Silva, Eric Swanson, Tanaporn Wangsanut, Kaycie Tayler, Brian Wiltgen, Asa Hatami, Raik Rönicke, Klaus Reymann, Birgit Hutter-Paier, Anca Alexandru, Wolfgang Jagla, Sigrid Graubner, Charles G. Glabe, Hans-Ulrich Demuth () and George S. Bloom ()
Additional contact information
Justin M. Nussbaum: University of Virginia
Stephan Schilling: Probiodrug AG, 06120 Halle (Saale), Germany
Holger Cynis: Probiodrug AG, 06120 Halle (Saale), Germany
Antonia Silva: University of Virginia
Eric Swanson: University of Virginia
Tanaporn Wangsanut: University of Virginia
Kaycie Tayler: University of Virginia
Brian Wiltgen: University of Virginia
Asa Hatami: University of California at Irvine
Raik Rönicke: Deutsches Zentrum fuer Neurodegenerative Erkrankungen, c/o Leibniz-Institut fuer Neurobiologie, 39118 Magdeburg, Germany
Klaus Reymann: Deutsches Zentrum fuer Neurodegenerative Erkrankungen, c/o Leibniz-Institut fuer Neurobiologie, 39118 Magdeburg, Germany
Birgit Hutter-Paier: JSW Life Sciences GmbH, A-8074 Grambach, Austria
Anca Alexandru: Ingenium Pharmaceuticals GmbH, 82152 Munich/Martinsried, Germany
Wolfgang Jagla: Ingenium Pharmaceuticals GmbH, 82152 Munich/Martinsried, Germany
Sigrid Graubner: Ingenium Pharmaceuticals GmbH, 82152 Munich/Martinsried, Germany
Charles G. Glabe: University of California at Irvine
Hans-Ulrich Demuth: Probiodrug AG, 06120 Halle (Saale), Germany
George S. Bloom: University of Virginia

Nature, 2012, vol. 485, issue 7400, 651-655

Abstract: It is shown that the formation of amyloid-β oligomers, one of the histopathological signatures of Alzheimer’s disease, can be triggered by small quantities of a specifically truncated and post-translationally modified version of amyloid-β.

Date: 2012
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DOI: 10.1038/nature11060

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