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. 2019 Aug 20;25(12):3380–3398. doi: 10.1038/s41380-019-0483-4

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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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Fig. 9 — Prolonged inhibition of PV interneurons reduces Aβ levels and amyloid plaques in APP/PS1-PV-Cre mice. a Immunohistochemistry with anti-Aβ (6E10, red) antibody in 23–25-week-old mCherry-expressing APP/PS1-PV-Cre mice (upper panel) and hM4Di-expressing APP/PS1-PV-Cre mice (lower panel) 8 weeks following prolonged treatment showing plaques in the hippocampus (white arrows). Scale bar: 100 μm (overview), 20 μm (inset). b, c APP/PS1-PV-Cre mice expressing hM4Di showed a significant reduction in the average number of Aβ-positive plaques compared with APP/PS1-PV-Cre control mice (b), but not in average plaques size (c) (Student’s t test: n = 4 mice per group, *p < 0.05). d Relative Aβ_1–40 (left panel) and Aβ_1–42 (right panel) levels in the hippocampus of 23–25-week-old APP/PS1-PV-Cre mice 8 weeks following prolonged CNO treatment (Student’s t test; n = 13 mice per group, *p < 0.05)