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. 2021 Jan 4;10:1. doi: 10.1186/s40035-020-00225-y

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© The Author(s) 2021

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 — Higher NPI-Q and shorter EYO of AD were associated with higher [¹⁸F]FDG uptake decline in DIAD mutation carriers. Statistical parametric map overlaid on a structural MRI scan shows regions in the PCC (a), vmPFC (b), bilateral parietal lobes (c) and right AI (d) where higher [¹⁸F]FDG uptake decline was found in cognitively normal DIAD mutation carriers with higher NPI-Q scores and shorter EYO of AD. The analysis was corrected for gender, education, APOE ε4 status and family mutation type (APP, PSEN1 and PSEN2) and multiple comparisons were corrected using random field theory at p < 0.001. AD: Alzheimer disease; AI: anterior insula; DIAD: dominantly inherited Alzheimer’s disease; EYO: estimated years to onset; [¹⁸F]FDG: [¹⁸F]fluorodeoxyglucose; NPI-Q: Neuropsychiatric Inventory; PCC: posterior cingulate cortex; vmPFC: ventromedial prefrontal cortex