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. 2020 Jul 29;15:44. doi: 10.1186/s13024-020-00387-3

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© The Author(s) 2020

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. 5 — Association of BIN1 peptides with AD pathology. a Association between the abundance of BIN1 peptides and amyloid (left) or tangles (right) after adjusting for the other form of AD-related pathology. b Effect size of BIN1 peptides localized in exon 7 in relation to the abundance of tangles: there is an inverse relationship between the two factors. c Graph illustrating the results of our mediation analyses which suggest that BIN1 exon 7 peptides (i.e LQAHLVAQTNLLR) play a role in the accumulation of tangles and do not have an independent effect on cognitive decline. d Association of BIN1 peptides with APOEε4. The threshold of significance is reported on the Y axis and is denoted by the horizontal dashed line as the -log of the FDR value (FDR < 0.05)