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. 2020 Aug 4;12:240. doi: 10.3389/fnagi.2020.00240

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Copyright © 2020 Qin, An, Xu, Qi, Wang, Chen, Chen and Sha.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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p75^NTR participates in E2-induced protection of NSC proliferation in APP/PS1 mice. (A,B) Influence of E2 on the level of p75^NTR in 6-month-old APP/PS1 mice. The upper panels represent representative blots of p75^NTR. Bar graphs show the level of p75^NTR protein or p75^NTR mRNA in APP/PS1 mice or OVX-APP/PS1 mice treated with vehicle or E2 for 2 months. **P < 0.01 vs. sham-op APP/PS1 mice; ^##P < 0.01 vs. OVX-APP/PS1 mice (two-way ANOVA). (C,D) Influence of the p75^NTR inhibitor TAPI-2 on the excessive proliferation of NSCs and survival of immature neurons in the DG of 6-month-old APP/PS1 mice. The bar graphs show the number of BrdU⁺ cells and the density of DCX⁺ cells in APP/PS1 mice or OVX-APP/PS1 mice treated with vehicle or TAPI-2 for 7 days. *P < 0.05 vs. sham-op APP/PS1 mice; ^#P < 0.05 vs. OVX-APP/PS1 mice (two-way ANOVA).