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. 2020 Sep 29;17:60. doi: 10.1186/s12987-020-00219-y

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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 — Differential content of laminin, TSG-6, and HA in MV isolated from no CAA and moderate to severe CAA brains. Western immunoblot assays showed that expression of laminin (a, inset of representative western blot) was significantly lower in lysates of MV isolated from no CAA brains vs. moderate-severe (Mod-Sev) CAA brains). Analyses of TSG-6 (b, inset of representative western blot) and HA (ELISA) content showed significant increases with moderate to severe CAA. Shown are scatter plots with mean and SEM, p values are as shown. Sample sizes (n) are indicated in “Results”