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. 2023 Mar 10;15:48. doi: 10.1186/s13195-023-01201-0

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© The Author(s) 2023

Open AccessThis 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. 3 — CSF levels of p-tau235 across AT groups. In both a the Paris cohort and b the BIODEGMAR cohort, CSF p-tau235 followed an increasing trajectory across the AT continuum. CSF p-tau235 was significantly increased in A+T+ when compared with A−T− and A+T−, and approached significance between A−T− and A+T− in the Paris cohort. Data information: Boxplots show the median, IQR, and all the participants colour-coded based on the presence (red) or absence (blue) of CSF amyloidosis measured with Lumipulse CSF Aβ_1–42/40. P-values were determined using one-way ANOVA adjusted by age and sex, followed by Bonferroni-corrected post hoc comparison (*P <0.05, **P <0.01, ***P <0.001, ****P <0.0001)