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. 2022 Jan 24;10:6. doi: 10.1186/s40478-021-01303-6

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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. 3 — The brain microvascular proteome of patients with Alzheimer’s disease. a Venn diagram demonstrating the overlap of 3780 proteins identified in at least 6 of the 13 samples from patients with Alzheimer’s disease (AD) and 6 of the 12 samples from control (CON) subjects. b Volcano plot illustrating log₂ LFQ ratios (AD vs CON) and − log10 p values of all quantified proteins. Blue symbols (n = 82) indicate proteins with a significant change in abundance (p < 0.05, log₂ ratio < − 1.0/ > 1.0). c Abundance distribution according to the mean iBAQ intensity for each protein. Significantly altered proteins are indicated in blue. The three most and least abundant proteins are labeled with gene names. d Protein localization of significantly altered proteins and of all identified proteins according to UniProt subcellular localization information