Constant Transmission Properties of Variant Creutzfeldt-Jakob Disease in 5 Countries
Abigail B. Diack, Diane Ritchie, Matthew Bishop, Victoria Pinion, Jean-Philippe Brandel, Stephane Haik, Fabrizio Tagliavini, Cornelia Van Duijn, Ermias D. Belay, Pierluigi Gambetti, Lawrence B. Schonberger, Pedro Piccardo, Robert G. Will1, and Jean C. Manson1
Author affiliations: The Roslin Institute, Easter Bush, Scotland, UK (A.B. Diack, V. Pinion, J.C. Manson); University of Edinburgh, Edinburgh, Scotland, UK (D. Ritchie, M. Bishop, R.G. Will); Cellule Nationale de Référence des Maladies de Creutzfeldt-Jakob, Universite Pierre et Marie Curie-Paris 6, INSERM, and CNRS, Paris, France (J.-P. Brandel, S. Haik); Fdazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy (F. Tagliavini); Erasmus University Medical School, Rotterdam, the Netherlands (C. Van Duijn); Centers for Disease Control and Prevention, Atlanta, Georgia, USA (E.D. Belay, L.B. Schonberger); Case Western Reserve University, Cleveland, Ohio, USA (P. Gambetti); and Food and Drug Administration, Rockville, Maryland, USA (P. Piccardo)
Figure 2. . Lesion profile comparison of variant Creutzfeldt-Jakob disease cases show similarities in vacuolar pathology levels and regional distribution in mouse brains. Wild-type mouse lines RIII (A), C57 (B), and VM (C) are shown. Data show mean lesion profile ± SEM (n>6). G1–G9, gray matter scoring regions: G1, dorsal medulla; G2, cerebellar cortex; G3, superior colliculus; G4, hypothalamus; G5, thalamus; G6, hippocampus; G7, septum; G8, retrosplenial and adjacent motor cortex; G9, cingulate and adjacent motor cortex. W1–W3, white matter scoring regions: W1, cerebellar white matter; W2, mesencephalic tegmentum; W3, pyramidal tract.
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