[Jiaotaiwan improves brain glucose metabolism in a mouse model of Alzheimer's disease by activating the PI3K/AKT signaling pathway].

Jun 11, 2024Nan fang yi ke da xue xue bao = Journal of Southern Medical University

Jiaotaiwan may improve brain sugar use in Alzheimer's mice by activating a key cell survival pathway

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Abstract

Treatment with Jiaotaiwan improved memory ability and increased hippocampal neuron counts in a mouse model of Alzheimer's disease.

AD mouse models showed significant learning and memory impairments, alongside increased Aβ amyloid plaques in the brain.
Fasting serum insulin levels were elevated, indicating insulin resistance, while key components of the insulin-PI3K/AKT pathway were reduced.
Treatment with Jiaotaiwan and donepezil resulted in reduced Aβ amyloid plaques and increased neuronal counts in the hippocampus.
Both treatments enhanced the expression of PI3K, AKT, and glucose transporters in brain regions associated with memory and learning.

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OBJECTIVE: To investigate the effect ofon brain insulin-PI3K/AKT pathway in a mouse model of Alzheimer's disease (AD). Jiaotaiwan

METHODS: Fifty 3-month-old male APP/PS1 double transgenic mice were randomized into AD model group, low-, medium- and high-dosetreatment groups, and donepezil treatment group. Cognitive functions of the mice were assessed using water maze and open field tests, and neuronal pathologies were observed with HE staining and Nissl staining; immunohistochemistry was used to detect amyloid Aβ deposition in the brain. Fasting serum insulin levels of the mice were measured, and the expressions of Aβ, insulin-PI3K/AKT pathway components and downstream glucose transporters in the brain tissue were detected with RT-qPCR and Western blotting. Jiaotaiwan42

RESULTS: The AD mouse models exhibited obvious impairment of learning and memory abilities, significantly reduced hippocampal neurons, and obvious Aβ amyloid plaques in the brain tissue with increased Aβprotein expression (< 0.05) and insulin resistance index, decreased hippocampal PI3K expressions, lowered expressions of AKT and InR, reduced expressions of GLUT1, GLUT3, and GLUT4, and increased expression of GSK3β in both the hippocampus and cortex. Treatment withand donepezil both effectively improved memory ability of the mouse models, increased the number of hippocampal neurons, reduced Aβ amyloid plaques and increased the expressions of PI3K, AKT, InR, GLUT1, GLUT3 and GLUT4 in the hippocampus and cortex. 42P Jiaotaiwan

CONCLUSION: improves learning and memory abilities of APP/PS1 double transgenic mice and delay the development of AD by activating the PI3K/AKT pathway and regulating the expression levels of its downstream GLUTs in the brain. Jiaotaiwan

[Jiaotaiwan improves brain glucose metabolism in a mouse model of Alzheimer's disease by activating the PI3K/AKT signaling pathway].

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