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. 2019 Feb 26;9:2827. doi: 10.1038/s41598-019-39494-7

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© The Author(s) 2019

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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BCAS decreased the concentrations of small molecular weight Aβ, and accelerated their apparent clearance in APP/PS1 mice. (a) Schematic view of the in vivo microdialysis apparatus. The guide cannula was stereotactically implanted into the hippocampus. The microdialysis probe, equipped with 1000 kDa semipermeable membrane, was inserted into the target region through the guide cannula. Artificial cerebrospinal fluid (aCSF) was circulated within the probe every hour and collected as interstitial fluid (ISF). Aβ concentration was measured by ELISA. (b,d) Time-series of the Aβ₄₀ and Aβ₄₂ concentration in each fraction. A gamma-secretase inhibitor, Compound E, was administered at the time point 0 to inhibit the local production of Aβ. (c,e) Half-life periods of Aβ₄₀ (c) and Aβ₄₂ (e) within the hippocampus of sham or BCAS-operated mice. The concentrations from 0 h to 4 h in panels b and d were replotted and normalized with baseline concentration. Half-life periods of Aβ_1–40 and Aβ_1–42 were determined as the slopes of the concentrations. Statistical significance was determined by two-way ANOVA.