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. 2021 Oct 19;12(1):8540–8554. doi: 10.1080/21655979.2021.1987082

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© 2021 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 2. — The distribution of Aβ, p-Tau and CD11b immunolabeling across the brains in the AD+TG, AD+donepezil, AD model and Normal control groups. (a–e): The distribution of Aβ immunolabeling in the AD+TG, AD+donepezil, AD model and Normal control groups. (f–j): The distribution of p-Tau immunolabeling in the AD+TG, AD+donepezil, AD model and Normal control groups. (k–o): The distribution of CD11b immunolabeling in the AD+TG, AD+donepezil, AD model and Normal control groups. Data was expressed as the mean ± standard error of the mean (SEM). (n = 8/group in the AD+TG group; n = 8/group in the AD+donepezil group; n = 8/group in the AD model group; n = 8/group in the Normal control group). ‘**’ indicating significant inter-group difference. TG: Tripterygium glycoside; AD: Alzheimer disease; NS: normal saline