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. 2022 Jun 17;13:261. doi: 10.1186/s13287-022-02933-w

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© The Author(s) 2022

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. 3 — SKN cell therapy triggers supraphysiological hippocampal synaptogenesis. A Chart showing synaptic density in hippocampus in therapeutic responders is specifically and markedly increased, 5–13 SDs higher (average ~ 9SD) than in non-treated aged animals (n = 10). Charts shows average ± 95%CI for untreated dogs. B No significance difference was observed in non-hippocampal areas. C Exemplar images from the CA3 stratum oriens subfield (SO, high and low magnification). Responders showed a remarkably high density of neurons positive for immature marker βIII tubulin (green) that are absent in non-treated CCD older dogs, as well as intense positivity for presynaptic synaptophysin (red, and co-labelled immature neuronal presynaptic punctae (yellow). Panels for CA1, CA3 stratum radiatum and dentate gyrus in Additional file 1: Figures S7–9