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. 2021 Jun 15;18:139. doi: 10.1186/s12974-021-02191-2

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© The Author(s) 2021

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. 8 — Microglia Ager deletion in male SOD1^G93A mice reduces the accumulation of disease-associated microglia at end-stage. a Representative images of CLEC7A staining in the lumbar spinal cord ventral horn of the indicated mouse groups. Scale bar: 50 μm. b Quantification of CLEC7A⁺ area. c Quantification of CLEC7A⁺ DAPI⁺ cell number. Mean ± SD. N = 7 SOD1^G93A Ager^fl/fl Cx3cr1^Cre/+ mice and N = 9 SOD1^G93A Ager^+/+ Cx3cr1^Cre/+ mice. Independent two sample two-sided t test. In b, **p < 0.0048. In c, *p = 0.0154