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Your search keyword '"Ke, Sujie"' showing total 2 results
Start Over Author "Ke, Sujie" Topic alzheimer disease
2 results on '"Ke, Sujie"'

1. Exenatide alleviates mitochondrial dysfunction and cognitive impairment in the 5×FAD mouse model of Alzheimer's disease.

Author

An J, Zhou Y, Zhang M, Xie Y, Ke S, Liu L, Pan X, and Chen Z

Subjects
Amyloid beta-Peptides metabolism, Amyloid beta-Protein Precursor metabolism, Animals, Brain metabolism, Disease Models, Animal, Exenatide metabolism, Glucagon-Like Peptide 1 metabolism, Glucagon-Like Peptide-1 Receptor agonists, Hippocampus metabolism, Male, Memory physiology, Mice, Mice, Inbred Strains, Mice, Transgenic, Mitochondria drug effects, Neuroprotective Agents pharmacology, Plaque, Amyloid metabolism, Synapses metabolism, Alzheimer Disease metabolism, Cognitive Dysfunction drug therapy, Exenatide pharmacology
Abstract

The role of mitochondrial dysfunction has been well-documented in Alzheimer's disease (AD). Glucagon-like peptide 1 (GLP-1) receptor agonists are being utilized as neuroprotectants in the treatment of various neurological disorders, including AD. We conducted this study to explore the effects of exenatide (a GLP-1 receptor agonist) on β-amyloid plaque (Aβ)-induced cognitive impairment and mitochondrial dysfunction in 5xFAD transgenic mice. Spatial memory test showed that exenatide administration (100 μg/kg twice per day) prevented cognitive decline after 16 weeks of treatment. Aβ 1-42 deposition and synapse damage in the hippocampus was significantly alleviated. Furthermore, exenatide treatment can improve mitochondrial morphology, relieve oxidative damage, correct mitochondrial energy crisis, and normalize mitochondrial dynamics. These findings suggest that exenatide, which has already been applied in clinical medicine, may be a promising agent for AD therapy via mitochondrial protection., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Published
2019
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2. Subcutaneous administration of liraglutide ameliorates learning and memory impairment by modulating tau hyperphosphorylation via the glycogen synthase kinase-3β pathway in an amyloid β protein induced alzheimer disease mouse model.

Author

Qi L, Ke L, Liu X, Liao L, Ke S, Liu X, Wang Y, Lin X, Zhou Y, Wu L, Chen Z, and Liu L

Subjects
Alzheimer Disease pathology, Alzheimer Disease physiopathology, Animals, Disease Models, Animal, Gene Expression Regulation drug effects, Glucagon-Like Peptide-1 Receptor metabolism, Hippocampus drug effects, Hippocampus physiopathology, Liraglutide administration & dosage, Liraglutide therapeutic use, Male, Maze Learning drug effects, Mice, Mice, Inbred C57BL, Neurons drug effects, Neurons ultrastructure, Phosphorylation drug effects, Proto-Oncogene Proteins c-akt metabolism, Spatial Learning drug effects, Synapses drug effects, Synapses metabolism, Alzheimer Disease drug therapy, Alzheimer Disease metabolism, Amyloid beta-Peptides pharmacology, Glycogen Synthase Kinase 3 beta metabolism, Liraglutide pharmacology, Memory drug effects, Peptide Fragments pharmacology, tau Proteins metabolism
Abstract

Type 2 diabetes mellitus is a risk factor for Alzheimer's disease (AD). The glucagon-like peptide-1 analog liraglutide, a novel long-lasting incretin hormone, has been used to treat type 2 diabetes mellitus. In addition, liraglutide has been shown to be neurotrophic and neuroprotective. Here, we investigated the effects of liraglutide on amyloid β protein (Aβ)-induced AD in mice and explored its mechanism of action. The results showed that subcutaneous administration of liraglutide (25nmol/day), once daily for 8 weeks, prevented memory impairments in the Y Maze and Morris Water Maze following Aβ1-42 intracerebroventricular injection, and alleviated the ultra-structural changes of pyramidal neurons and chemical synapses in the hippocampal CA1 region. Furthermore, liraglutide reduced Aβ1-42-induced tau phosphorylation via the protein kinase B and glycogen synthase kinase-3β pathways. Thus liraglutide may alleviate cognitive impairment in AD by at least decreasing the phosphorylation of tau., (Copyright © 2016 Elsevier B.V. All rights reserved.)

Published
2016
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