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. 2011 Dec 12;108(52):21223–21228. doi: 10.1073/pnas.1117827108

Fig. 4.

Fig. 4.

Neuropathologic analysis of spontaneously ill Tg(PrP,ΔGPI:PrP)8015/4053 mice. (A–I) Brain sections taken from the hippocampus (Left), thalamus (Center), and cerebellum (Right) were examined for neuropathologic changes. (A–C) Immunostaining with anti-PrP Fab R2 showed that PrP deposits were abundant in the hippocampus, sparse in the thalamus, and absent in the cerebellum. (D–F) ThioS staining demonstrated that some of the PrP deposits could be classified as amyloid. (G–I) H&E staining showed only little or no vacuolation. Overall, the neuropathology was less severe than that observed in ill Tg8015/Prnp0/0 mice. (Scale bar: A–I, 50 μm.) (J–L) Double-fluorescence labeling of brain sections with ThioS (J) and anti-myc tag antibody (K) showed coincidence (L), indicating that amyloid plaques from Tg mice coexpressing PrP(ΔGPI) and PrPC contain PrP(ΔGPI). (Scale bar: J–L, 100 μm.)