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. 2023 May 4;18:31. doi: 10.1186/s13024-023-00611-w

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© The Author(s) 2023

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. 9 — Targeted astrocytic deletion of Bace1 reduces amyloid plaques by increasing Aβ clearance. A Thioflavin-S staining of amyloid plaques from saggital brain sections of 5xFAD;Bace1^fl/fl;Gfap-cre and 5xFAD;Bace1^fl/fl. Scale bar indicates 100 µm (B) Quantification of Thioflavin-S positive amyloid plaques calculated by counting serial sagittal sections, which were selected at 10-section intervals (N = 7 for 5xFAD;Bace1^fl/fl;Gfap-cre and 5xFAD;Bace1^fl/fl). C Western blot of cortical lysates from 5xFAD;Bace1^fl/fl;Gfap-cre and 5xFAD;Bace1^fl/fl mice. Images indicate APP full length, APP C-terminal C99 (detected by 6E10) and C99/C83 bands (detected by APP A8717 antibody). Actin was included as loading control