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. 2020 Jan 30;11:619. doi: 10.1038/s41467-020-14373-2

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© The Author(s) 2020

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — a LCN2 immunohistochemistry in the cerebral cortex of control, Alzheimer’s disease (AD), and Multi-Infarct Chronic Encephalopathy (MID) cases, including subacute infarct areas (MID-SAI area) and astrocytic scar areas (MID-AS area). LCN2 staining is observed in intact blood vessels in controls, AD and MID cases (arrow-heads). Increased LCN2 expression is observed in reactive astrocytes in AD and MID (arrows) and in monocyte/macrophage cells of the MID-SAI area (empty arrow-heads). Paraffin sections counterstained with hematoxylin. Bar: 25 µm; insert-bar 50 µm. b Quantification of LCN2 positive cells area in cerebral cortex and striatum in µm². Significant increase of LCN2 positive cells area in MID cases with respect to controls (***p < 0.001) and AD cases (*p < 0.05). Shown results are means (±SD) of controls (n = 11), AD (n = 10), and MID (n = 11) cases. In MID cases, area of subacute infraction (n = 6) and chronic infarcts (n = 11) were analysed. Results were analysed by Kruskal-Wallis followed by Dunn's Multiple Comparison test.