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. 2022 Mar 29;14:46. doi: 10.1186/s13195-022-00990-0

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© The Author(s) 2022

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. 1 — Comparisons of plasma biomarkers between MCI who progressed to AD dementia and those who did not. Levels of plasma p-tau217 (A), NfL (B), Aβ42/Aβ40 ratio (C), and GFAP (D) between MCI patients who did not progress to AD dementia (non-progressors) vs. those who progressed to AD dementia (progressors) within 3 years. Boxes represent the first and third quartile of each distribution, and whiskers extend up to 1.5-times the interquartile range. Corresponding p-value and Cohen’s d effect size are reported on the top of each panel. Aβ, beta-amyloid; GFAP, glial fibrillary acidic protein; NfL, neurofilament light; MCI, mild cognitive impairment; p-tau217, phosphorylated tau 217