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. 2023 Jul 11;28(12):5380–5389. doi: 10.1038/s41380-023-02166-0

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© The Author(s) 2023

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. 3 — Scale bar 50 μm. A IV:5 and (B) IV:3; both patients carry the TRL9 p.E317D variant, (C) and (D) are AD patients with PSEN1 p.P264L and p.I143T respectively, (E) and (F) are two sporadic AD patients and (G) and (H) are neurologically healthy controls. The TLR9 p.E317D mutation carriers (Fig. 3A, B) and the other AD (C–F) showed alterations of microglia morphology. In the TLR9 p.E317D (A, B) the microglia cells appeared more condensed with less processes and ramifications and with the least overlap in microglia territory.