Spontaneous Generation of Infectious Prion Disease in Transgenic Mice
Juan-María Torres
, Joaquín Castilla, Belén Pintado, Alfonso Gutiérrez-Adan, Olivier Andréoletti, Patricia Aguilar-Calvo, Ana-Isabel Arroba, Beatriz Parra-Arrondo, Isidro Ferrer, Jorge Manzanares, and Juan-Carlos Espinosa
Author affiliations: Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria, Madrid, Spain (J.-M. Torres, J. Castilla, B. Pintado, A. Gutiérrez-Adán P. Aguilar-Calvo, A.-I. Arroba, B. Parra-Arrondo, J.-C. Espinosa); Basque Foundation for Science, Bilbao, Spain (J. Castilla); Ecole Nationale Vétérinaire de Toulouse, Toulouse, France (O. Andréoletti); Hospitalet de Llobregat, Barcelona, Spain (I. Ferrer); Universidad Miguel Hernandez, Sant Joan d´Alacant, Spain (J. Manzanares)
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Figure 2
Figure 2. . . Comparison between homozygous bovine prion protein (BoPrP)-Tg110+/+ control mice (panels A–D) and hemizygous 113LBoPrP-Tg037+/− mice with end-stage disease (panels E–H) in parietal cortex (panels A and E), CA1 region of the hipocampus (panels B and F), dentate gyrus (panels C and G), and medial thalamus (panels D and H). Severe spongiosis is seen in the cerebral cortex, hilus ofdentate gyrus, and medial thalamus, but not in the CA1 area of the hippocampus and granule cell layer of the dentate gyrus. 113L, leucine substitution at codon 113. Paraffin-embedded sections were stained with hematoxylin and eosin. Scale bar in panel H = 25 μm.
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