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. 2020 Apr 7;12:40. doi: 10.1186/s13195-020-00607-4

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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 — Amyloid pathology is reduced by EMP treatment. a SP burden was lower in APP/PS1xdb/db mice when compared with APP/PS1 animals. EMP treatment slightly reduced SP burden in the cortex after TS and 4G8 staining (TS [F_{(3, 107)} = 20.55], 4G8 [F_{(3, 104)} = 11.89]; ^††p < 0.01 vs. APP/PS1 and APP/PS1-EMP). While individual SP size was increased in APP/PS-EMP mice (TS [F_{(3, 5191)} = 8.98], 4G8 [F_{(3, 5039)} = 21.11]; ^‡‡p < 0.01 vs. APP/PS1-EMP; ^††p < 0.01 vs. APP/PS1 and APP/PS1-EMP), EMP treatment reduced SP density (TS [F_{(3, 107)} = 19.74], 4G8 [F_{(3, 107)} = 17.81]; ^‡‡p < 0.01 vs. APP/PS1; ^††p < 0.01 vs. APP/PS1 and APP/PS1-EMP). To a lesser extent, we observed a similar trend when we analyzed SP burden in the hippocampus (TS [F_{(3, 49)} = 8.01], 4G8 [F_{(3, 49)} = 6.08]; ^‡‡p < 0.01 vs. APP/PS1]), SP density (TS [F_{(3, 50)} = 11.57], 4G8 [F_{(3, 50)} = 9.42]; ^‡‡p < 0.01 vs. APP/PS1), and individual plaque size (TS [F_{(3, 643)} = 0.975, p = 0.404]; 4G8 [F_{(3, 638)} = 2.39, p = 0.067]) (APP/PS1 n = 5, APP/PS1-EMP n = 5, APP/PS1xdb/db n = 5, APP/PS1xdb/db-EMP n = 5). b Illustrative example of cortical regions stained with TS and 4G8 where reduced SP density can be observed after EMP treatment. Scale bar = 50 μm. c A similar profile was observed in the hippocampus when we measured SP burden, density, and individual SP size (^‡‡p < 0.01 vs. APP/PS1) (APP/PS1 n = 5, APP/PS1-EMP n = 5, APP/PS1xdb/db n = 5, APP/PS1xdb/db-EMP n = 5). d EMP treatment reduced soluble Aβ40 levels in the cortex ([F_{(3, 27)} = 4.20, ^‡p = 0.015 vs. APP/PS1xdb/db]). While a similar trend was observed in the hippocampus, differences were not statistically significant ([F_{(3, 26)}=0.479, p = 0.7]). No differences were observed for soluble Aβ42 levels in the cortex ([F_{(3, 27)} = 0.832, p = 0.488]) or the hippocampus ([F_{(3, 26)} = 1.02, p = 0.397]). EMP also reduced insoluble Aβ40 levels in the cortex ([F_{(3, 25)} = 5.98, **p = 0.003 vs. the rest of the groups]), while differences did not reach statistical significance for insoluble Aβ40 in the hippocampus ([F_{(3, 22)} = 2.68, p = 0.072]) as well as for insoluble Aβ42 levels (cortex [F_{(3, 27)} = 1.43, p = 0.254]; hippocampus [F_{(3, 26)} = 1.54, p = 0.228]) (APP/PS1 n = 7, APP/PS1-EMP n = 9, APP/PS1xdb/db n = 7, APP/PS1xdb/db-EMP n = 7)