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. 2023 May 15;29(5):1243–1252. doi: 10.1038/s41591-023-02318-3

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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 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. 6 — a,b, Graphic representation and representative images of the distribution and intensity of pTau (a) and Aβ (b) pathology signals with normalized minimum and maximum values shown in red and blue, respectively in the cases with RELN-COLBOS and APOECh. The case with APOECh showed distinct decreased pTau pathological profiles in all cortices compared to the case with RELN-COLBOS. Despite some distribution differences, the Aβ pathology profile was similarly severe in both cases. AMY, amygdala; CAU, caudate; CNG, cingulate cortex; IPC, inferior parietal cortex; ITC, inferior temporal cortex; MES, mesencephalon; MFC, medial frontal cortex; MTC, middle temporal cortex; OL, occipital lobe; PUT, putamen; STC, superior temporal cortex; THA, thalamus. Scale bars, 250 μm.