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. 2021 Aug 31;6:325. doi: 10.1038/s41392-021-00748-4

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© The Author(s) 2021

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. 5 — Overexpression of ACAA1 p.N299S in APP/PS1ΔE9 mice and WT littermates induced neuronal losses. a, b Neuronal loss in the CA3 region of hippocampus in WT littermates (a) and APP/PS1ΔE9 mice (b) after delivery of the AAV-Vector, AAV-ACAA1 WT, and AAV-ACAA1 N299S. Higher neuronal density, marked by NeuN antibody, was noted in mice overexpressing ACAA1 p.N299S, suggesting a potential decrease of neurogenesis or an increase of neuron loss. Immunostaining of brain sections was performed using NeuN antibody. Shown results are representative hematoxylin and eosin (H&E) staining (top), Nissl staining (middle), and NeuN staining (bottom) of mouse hippocampus tissues in each group. c, d Decreased protein levels of structural plasticity markers SYP, PSD95, NeuN, GluR1, GluR1 (pS831), and GRIN2B in the hippocampus tissues of WT littermates (c) and APP/PS1ΔE9 (d) mice with AAV-mediated expression of ACAA1 and its mutant. Bars represent mean ± SD. ns, not significant; *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001; Student’s t test