ArticleMolecular neurobiology2016
Activation of mTOR signaling mediates the increased expression of AChE in high glucose condition: in vitro and in vivo evidences.
Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 36 citations in OpenAlex.
- Rewiring mTOR signaling in Alzheimer's disease: emerging mTOR modulators beyond oncology.Bioscience reports · 2026Review
- Investigating the Potential Therapeutic Mechanisms of Puerarin in Neurological Diseases.Molecular neurobiology · 2024Review
- Oxidative Stress Triggers a Pivotal Peptide Linked to Alzheimer's Disease.International journal of molecular sciences · 2024Article
- Cellular Metabolism: A Fundamental Component of Degeneration in the Nervous System.Biomolecules · 2023Review
- mTOR-dependent TFEB activation and TFEB overexpression enhance autophagy-lysosome pathway and ameliorate Alzheimer's disease-like pathology in diabetic encephalopathy.Cell communication and signaling : CCS · 2023Article
- Resveratrol ameliorates the behavioural and molecular changes in rats exposed to uninephrectomy: role of hippocampal SIRT1, BDNF and AChE.Journal of physiology and biochemistry · 2023Article
- The Metabolic Basis for Nervous System Dysfunction in Alzheimer's Disease, Parkinson's Disease, and Huntington's Disease.Current neurovascular research · 2023Article
- Article
- Metformin Protects Against Diabetes-Induced Cognitive Dysfunction by Inhibiting Mitochondrial Fission Protein DRP1.Frontiers in pharmacology · 2022Article
- The mTOR/NF-κB Pathway Mediates Neuroinflammation and Synaptic Plasticity in Diabetic Encephalopathy.Molecular neurobiology · 2021Article
- New Insights for nicotinamide: Metabolic disease, autophagy, and mTOR.Frontiers in bioscience (Landmark edition) · 2020Review
- Dysregulation of metabolic flexibility: The impact of mTOR on autophagy in neurodegenerative disease.International review of neurobiology · 2020Review
- Nicotinamide: Oversight of Metabolic Dysfunction Through SIRT1, mTOR, and Clock Genes.Current neurovascular research · 2020Review
- Enhancement of glyoxalase 1, a polyfunctional defense enzyme, by quercetin in the brain in streptozotocin-induced diabetic rats.Naunyn-Schmiedeberg's archives of pharmacology · 2018Article
- Neuroprotective Effects and Mechanisms of Tea Bioactive Components in Neurodegenerative Diseases.Molecules (Basel, Switzerland) · 2018Review
- Sarsasapogenin suppresses Aβ overproduction induced by high glucose in HT-22 cells.Naunyn-Schmiedeberg's archives of pharmacology · 2018Article
- Gastrodin Ameliorates Cognitive Dysfunction in Diabetes Rat Model via the Suppression of Endoplasmic Reticulum Stress and NLRP3 Inflammasome Activation.Frontiers in pharmacology · 2018Article
- Article
- AGEs and neurodegeneration: the Nrf2/glyoxalase-1 interaction.Oncotarget · 2017Article
- Targeting molecules to medicine with mTOR, autophagy and neurodegenerative disorders.British journal of clinical pharmacology · 2016Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acetylcholinesterase (AChE) is impaired in brain of diabetic animals, which may be one of the reasons for diabetes-associated cognitive decline. However, the mechanism is still unknown. The present study was designed to investigate whether the increased expression of AChE in central neurons under high glucose (HG) condition was due to activation of mammalian target of rapamycin (mTOR) signaling. It was found that more production of reactive oxygen species, and higher levels of phospho-Akt, phospho-mTOR, phospho-p70S6K, and AChE were detected in HT-22 cells in HG group than normal glucose group after culture for 24 h, which were all attenuated by an antioxidant N-acetyl-L-cysteine. A PI3K inhibitor LY294002 significantly decreased the levels of phospho-Akt, phospho-mTOR, phospho-p70S6K, and AChE protein expression in HG-cultured HT-22 cells, and an mTOR inhibitor rapamycin markedly reduced the levels of phospho-mTOR, phospho-p70S6K, and AChE expression. Furthermore, compared with normal rats, diabetic rats showed remarkable increases in levels of AChE activity and expression, malondialdehyde, phospho-mTOR, phospho-p70S6K, and a significant decrease in total superoxide dismutase activity in both hippocampus and cerebral cortex. However, much lower levels of phospho-mTOR, phospho-p70S6K, and AChE expression occurred in both brain regions of diabetic rats treated with rapamycin when compared with untreated ones. These results indicated that mTOR signaling was activated through the activation of PI3K/Akt pathway mediated by oxidative stress in HG-cultured HT-22 cells and diabetic rat brains, which contributed to the elevated protein expression of AChE in central neurons under the condition of HG.
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