Figure 1
From: Transmission of scrapie prions to primate after an extended silent incubation period

Neuropathological features of scrapie-infected cynomolgus macaque.
A) Macroscopic view of brain atrophy predominant in temporal lobe and enlarged ventricles, associated with a half-turn rotation of the hippocampal formation (x 1.4, Klüver-Barrera (KB) stain). (B) Laminar spongiform change involving mostly layer IV of occipital cortex (x 100 original magnification, Hematoxylin-Eosin (HE)). (C) Spongiform change in Purkinje cells of the cerebellar cortex, most of them being shrunken or absent (x 400, KB). (D) Axonal loss of the temporal white matter, visualized with monoclonal anti-neurofilament antibody 2F11 (x 400, 2F11 antibody), in comparison to (E) a normal neurofilament staining in temporal white matter of a healthy primate (x 400). (F) Massive lesion of the dorso-medialis thalamic nucleus (x 25, KB) (G) Higher magnification of the thalamic nucleus (corresponding to the inset in panel (F) showing massive rarefaction of neurons (arrows marked the few remaining neurons), an increase of the density of glia and spongiosis (x 400, KB), in comparison to (H) the same thalamic region in healthy primate. (I) Higher magnification of the laminar spongiosis of occipital cortex (x200, HE), in comparison to (J) the occipital cortex of healthy primate (x200, HE). (K) Iron deposits in the globus pallidus (x 400, Perls).