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. 2017 Nov 2;8:1268. doi: 10.1038/s41467-017-01347-0

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — Distinct disease phenotypes observed in affected mice following intravenous exposure to vCJD-contaminated products. a Synopsis of the distribution of lesions and biochemical features in the central nervous system (CNS) of mice depending on the disease phenotype. Small dots indicate the presence of only neuronal lesions (mainly vacuolation), large dots indicate sponJPEGorm change (plus neuronal lesions) and the orange colour indicates the presence of abnormal PrP^d. The respective numbers of cases are reported (N). vCJD phenotype: b classical spongiform change (hemalun–eosine, H&E stain, 200×) and c abnormal PrP^d deposition (Saf-32 anti-PrP antibody, 50×). Bulbospinal phenotype (BS): d spongiform changes were limited to the brainstem and spinal cord without cerebral involvement. Spinal phenotype (S): e spongiform change was limited to part or all of the spinal cord (H&E stain, 200×) but d no obvious brain lesion. f Accumulation of PrP^d in the spinal cord and dorsal roots was detected by immunohistochemistry in those 10 animals and the 16 aging spinal (AS) mice. Cerebral phenotype (C): moderate neuronal lesions and h cerebral spongiform change (H&E stain, 200×) with g a topographical distribution similar to vCJD mice (among them, 9 animals exhibited spongiform change limited to the brainstem, and were sub-grouped under the brainstem phenotype, or B). i They exhibited no accumulation of peripheral or central PrP^d (Saf-32 anti-PrP antibody, 200×) that was detectable using conventional techniques (ELISA, western blot and/or immunohistochemistry). Neuronal lesions only phenotype (NL): six animals showed apoptotic neurons with vacuolation in the brain (j) without spongiform change or detectable accumulation of PrP^d. Mean (+standard deviation) spongiosis profiles (d, g, j) observed for the different disease profiles. The horizontal line corresponds to the limit of significance. DM dorsal medulla, ND nucleus dentatus, CC cerebellar cortex, SC superior colliculus, HYP hypothalamus, THAL thalamus, STR striatum, HIPP hippocampus, SEPT septum, TC temporal cortex, PC parietal cortex, CSC cervical spinal cord, TSC thoracic spinal cord, LSC lumbar spinal cord. k Survival time distribution of neurologically affected mice according to their disease phenotypes. Red and white lines indicate the means and medians, respectively (the black star over spinal phenotype correspond to the 16 AS animals)