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. 2019 Jan 12;11:6. doi: 10.1186/s13195-018-0461-0

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© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 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.

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Fig. 8 — Aβ analyses. Brain homogenates from mice harvested at 8 M post-TBI were serially extracted in carbonate and then guanidine HCl (GuHCl) buffer. a The concentration of Aβ40 and Aβ42 in the GuHCl-soluble fraction is plotted. b The concentration of Aβ40 and Aβ42 in the carbonate-soluble fraction is plotted. c Using an Octet RED system with streptavidin biosensors, the levels of aducanumab-binding high-molecular-weight oligomeric and soluble fibril fragment forms of Aβ and the total level of Poly8029-binding Aβ were assayed. Human IgG1 served as an isotype control for aducanumab. Data are plotted as mean ± SE with an overlaid scatterplot of individual animals