The Neuroprotective Effects of SIRT1 in Mice Carrying the APP/PS1 Double-Transgenic Mutation and in SH-SY5Y Cells Over-Expressing Human APP670/671 May Involve Elevated Levels of α7 Nicotinic Acetylcholine Receptors

Cao, Kejiang; Dong, Yang-Ting; Xiang, Jie; Xu, Yi; Li, Yang; Song, Hui; Yu, Wenbin; Qin, Xiaolan; Guan, Zhi‐Zhong

doi:10.2139/ssrn.3422977

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“…In this context, the level of α7 nAChR is lowered in animal models of AD and in neurons treated with AβOs and, moreover, the loss of the ability of learning and memory of APP/PS1 mice can be reversed or aggravated by activating or inhibiting the expression of α7 nAChR, respectively [63,64]. Aβ damages nAChRs, and in particular α7 nAChR, directly, thereby altering neuronal signaling and contributing to the synaptic dysfunction associated with AD.…”

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confidence: 99%

The Mechanism by Which LiCl Attenuates the Impaired Ability of Learning and Memory of APP/PS1 Double Transgenic Mice May Involve Elevating the Expression of a7 Nicotinic Acetylcholine Receptors via Regulation of the Wnt/β-catenin Pathway

Xiang

Yan

Xiao

et al. 2021

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BackgroundWe examined the mechanism by which lithium chloride (LiCl) attenuates the impaired learning and memory of APP/PS1 double transgenic (APP/PS1) mice. MethodsSix- or twelve-month-old APP/PS1 and wild-type (WT) mice were divided randomly into 4 groups: 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 β-amyloid peptide oligomers (AβOs), LiCl and/or XAV939 (inhibitor of Wnt/β-catenin) or transfected with small interfering RNA against the β-catenin gene. Phosphor-glycogen synthase kinase-3β (GSK3β) (ser9), total GSK3β, β-catenin, cyclin D1, and α7 nAChR protein and mRNA were quantified by Western blotting or real-time PCR, respectively; senile plaques and α7 protein by immunohistochemical or immunofluorescent staining; Aβ 42 by ELISA; and cell viability by CCK8. Learning and memory were assessed utilizing the Morris water maze test. ResultsIn the brains of APP/PS1 mice, the level of Aβ was increased and those of α7 nAChR, phosphor-GSK3β (ser9), β-catenin, and cyclin D1 (at the protein and/or mRNA level) reduced. Treatment with LiCl for 2 months at 4 or 10 months of age attenuated all of these effects. Similar changes in the levels of these proteins were observed in primary neurons exposed to AβOs and these effects were attenuated by LiCl and aggravated by XAV939. Inhibition of β-catenin expression lowered the level of α7 nAChR protein in these cells. ConclusionLiCl attenuates the impaired ability of learning and memory of APP/PS1 mice via a mechanism that might involve elevation of the level of α7 nAChR as a result of altered Wnt/β-catenin signaling.

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Section: Discussionmentioning

confidence: 99%

The Mechanism by Which LiCl Attenuates the Impaired Ability of Learning and Memory of APP/PS1 Double Transgenic Mice May Involve Elevating the Expression of a7 Nicotinic Acetylcholine Receptors via Regulation of the Wnt/β-catenin Pathway

Xiang

Yan

Xiao

et al. 2021

Preprint

Self Cite

View full text Add to dashboard Cite

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The Neuroprotective Effects of SIRT1 in Mice Carrying the APP/PS1 Double-Transgenic Mutation and in SH-SY5Y Cells Over-Expressing Human APP670/671 May Involve Elevated Levels of α7 Nicotinic Acetylcholine Receptors

Cited by 1 publication

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The Mechanism by Which LiCl Attenuates the Impaired Ability of Learning and Memory of APP/PS1 Double Transgenic Mice May Involve Elevating the Expression of a7 Nicotinic Acetylcholine Receptors via Regulation of the Wnt/β-catenin Pathway

The Mechanism by Which LiCl Attenuates the Impaired Ability of Learning and Memory of APP/PS1 Double Transgenic Mice May Involve Elevating the Expression of a7 Nicotinic Acetylcholine Receptors via Regulation of the Wnt/β-catenin Pathway

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The Neuroprotective Effects of SIRT1 in Mice Carrying the APP/PS1 Double-Transgenic Mutation and in SH-SY5Y Cells Over-Expressing Human APP670/671 May Involve Elevated Levels of α7 Nicotinic Acetylcholine Receptors

Cited by 1 publication

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The Mechanism by Which LiCl&nbsp;Attenuates the Impaired Ability of Learning and Memory of APP/PS1 Double Transgenic Mice May Involve Elevating the Expression of a7 Nicotinic Acetylcholine Receptors via Regulation of the Wnt/β-catenin Pathway

The Mechanism by Which LiCl&nbsp;Attenuates the Impaired Ability of Learning and Memory of APP/PS1 Double Transgenic Mice May Involve Elevating the Expression of a7 Nicotinic Acetylcholine Receptors via Regulation of the Wnt/β-catenin Pathway

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The Mechanism by Which LiCl Attenuates the Impaired Ability of Learning and Memory of APP/PS1 Double Transgenic Mice May Involve Elevating the Expression of a7 Nicotinic Acetylcholine Receptors via Regulation of the Wnt/β-catenin Pathway

The Mechanism by Which LiCl Attenuates the Impaired Ability of Learning and Memory of APP/PS1 Double Transgenic Mice May Involve Elevating the Expression of a7 Nicotinic Acetylcholine Receptors via Regulation of the Wnt/β-catenin Pathway