BSE-associated Prion-Amyloid Cardiomyopathy in Primates
Susanne Krasemann, Giulia Mearini, Elisabeth Krämer, Katja Wagenführ, Walter Schulz-Schaeffer, Melanie Neumann, Walter Bodemer, Franz-Josef Kaup, Michael Beekes, Lucie Carrier, Adriano Aguzzi1, and Markus Glatzel1
Author affiliations: University Medical Center Hamburg-Eppendorf, Hamburg, Germany (S. Krasemann, G. Mearini, E. Krämer, M. Neumann, L. Carrier, M. Glatzel); Robert Koch Institute, Berlin, Germany (K. Wagenführ, M. Beekes); University Hospital Göttingen, Göttingen, Germany (W. Schulz-Schaeffer); German Primate Center, Göttingen (W. Bodemer, F.-J. Kaup); University of Zurich, Zurich, Switzerland (A. Aguzzi)
Figure 1. . PrPSc distribution and content in brain of bovine spongiform encephalopathy (BSE)–infected rhesus macaques. A) Paraffin-embedded tissue blot of striatum and cerebellum show a typical BSE-like deposition pattern of PrPSc with no differences between individual BSE-diseased monkeys at 49, 59, and 61 months postinoculation (mpi). Scale bars = 1 mm. B) Western blot analysis for PrPSc in brain of BSE-infected monkeys with incubation times of 49, 59, and 61 mpi. PrPSc-type is as expected for BSE prions, and no major differences in PrPSc load were detected. All samples were proteinase K–digested; loading amount was 0.5 and 0.1 mg fresh wet tissue for each sample
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