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. 2023 Aug 31;11:141. doi: 10.1186/s40478-023-01631-9

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© The Author(s) 2023

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 2 — Lesion profiles of 9 sCJDMV histotypes, and histopathology of 1C. a sCJD MV1/MV1-2 can be divided into two major groups. The first one includes 1C, 1V and 1C-2C histotypes, characterized by the sparing of the substantia nigra (SN) and less severe pathological changes in thalamic (TH) nuclei; the second group encompasses 1C-2PL & 1C-2K showing more severe lesions of SN and TH, and accumulation of plaque-like PrP deposits (1C-2PL) and PrP plaques (1C-2K). b Lesion profiles of MV2-1 show three major groups: 2C with sparing of SN, 2C-PL with mild lesions of SN, and 2C-K & 2K with overall different lesion profiles, and marked hippocampal pathology; the 2C-K histotype shows C and K histotypic features in the proportion of ~ 50% each. Dashed double arrows point to differences in severity in key brain regions. c–e, j Hematoxylin–eosin (H&E). f–i PrP immunostaining. c–e Spongiform degeneration affecting the neocortex (c) and subcortical regions (d) regions, but not the hippocampus (e). f–h Diffuse PrP; arrow, f a larger PrP granule. Mol. L.: Molecular layer; Grl. L.: granular layer. i A focus of coarse PrP. j H&E preparation stained for PrP in i; antibody: 3F4; dis. durat.: disease duration