| First Author | Xiang J | Year | 2021 |
| Journal | J Cell Mol Med | Volume | 25 |
| Issue | 22 | Pages | 10698-10710 |
| PubMed ID | 34708522 | Mgi Jnum | J:348531 |
| Mgi Id | MGI:6826629 | Doi | 10.1111/jcmm.17006 |
| Citation | Xiang J, et al. (2021) LiCl attenuates impaired learning and memory of APP/PS1 mice, which in mechanism involves alpha7 nAChRs and Wnt/beta-catenin pathway. J Cell Mol Med 25(22):10698-10710 |
| abstractText | We examined the mechanism by which lithium chloride (LiCl) attenuates the impaired learning capability and memory function of dual-transgenic APP/PS1 mice. Six- or 12-month-old APP/PS1 and wild-type (WT) mice were randomized into four groups, namely WT, WT+Li (100 mg LiCl/kg body weight, gavage once daily), APP/PS1 and APP/PS1+Li. Primary rat hippocampal neurons were exposed to beta-amyloid peptide oligomers (AbetaOs), LiCl and/or XAV939 (inhibitor of Wnt/beta-catenin) or transfected with small interfering RNA against the beta-catenin gene. In the cerebral zone of APP/PS1 mice, the level of Abeta was increased and those of alpha7 nicotinic acetylcholine receptors (nAChR), phosphor-GSK3beta (ser9), beta-catenin and cyclin D1 (protein and/or mRNA levels) reduced. Two-month treatment with LiCl at ages of 4 or 10 months weakened all of these effects. Similar expression variations were observed for these proteins in primary neurons exposed to AbetaOs, and these effects were attenuated by LiCl and aggravated by XAV939. Inhibition of beta-catenin expression lowered the level of alpha7 nAChR protein in these cells. LiCl attenuates the impaired learning capability and memory function of APP/PS1 mice via a mechanism that might involve elevation of the level of alpha7 nAChR as a result of altered Wnt/beta-catenin signalling. |
