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. 2022 Nov 30;14:1013891. doi: 10.3389/fnagi.2022.1013891

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Copyright © 2022 Zeng, Liu, Wang, Ye, Sun, Su, Qiu, Li, Wang, Wang, Ma, Li and Tian.

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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The gene basis for the cognitive impairment in kidney deficiency. (A) PCA displays sample clustering within age-matched control (n = 13) and AD hippocampal brain samples (n = 10). (B) Volcano plot of DEGs between the AD and control brain. The threshold parameters used were | Log₂ (fold change)| > 1 and p adjust < 0.05. (C) Venn diagram showing the shared genes among AO targets, DEGs and AD pathway (hsa05010). (D) Clustering heatmap of 66 AO targets differentially expressed in AD hippocampus. Red and green represent high and low expressed genes, respectively. The Top 10 AO-regulated DEGs ranked by degree with an asterisk in the heatmap were marked red (D). (E) 665 DEGs directly interact with 66 AO-regulated DEGs as shown in the PPI network. (F) CTNNB1 (β-catenin) directly interacts with 28 AO-regulated DEGs.