ArticleNeurobiology of aging2014
β-amyloid impairs the regulation of N-methyl-D-aspartate receptors by glycogen synthase kinase 3.
Article in Neurobiology of aging, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
28 citing papers in PubMed, 50 citations in OpenAlex.
- Unveiling the role of Na⁺/K⁺-ATPase pump: neurodegenerative mechanisms and therapeutic horizons.Pharmacological reports : PR · 2025Review
- RhoA/ROCK/GSK3β Signaling: A Keystone in Understanding Alzheimer's Disease.Current issues in molecular biology · 2025Review
- The mTOR Pathway: A Common Link Between Alzheimer's Disease and Down Syndrome.Journal of clinical medicine · 2024Review
- Correlation between obesity and AlzheimerZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Review
- Altered synaptic currents, mitophagy, mitochondrial dynamics in Alzheimer's disease models and therapeutic potential of Dengzhan Shengmai capsules intervention.Journal of pharmaceutical analysis · 2024Article
- Pathological Interplay between Inflammation and Mitochondria Aggravates Glutamate Toxicity.International journal of molecular sciences · 2024Review
- Bioinformatic analysis of hippocampal histopathology in Alzheimer's disease and the therapeutic effects of active components of traditional Chinese medicine.Frontiers in pharmacology · 2024Article
- The role of glycogen synthase kinase 3 beta in neurodegenerative diseases.Frontiers in molecular neuroscience · 2023Review
- Temporal Pattern of Neuroinflammation Associated with a Low Glycemic Index Diet in the 5xFAD Mouse Model of Alzheimer's Disease.Molecular neurobiology · 2022Article
- Ameliorative effect of carveol on scopolamine-induced memory impairment in rats.Iranian journal of basic medical sciences · 2022Article
- Role of Aβ in Alzheimer's-related synaptic dysfunction.Frontiers in cell and developmental biology · 2022Review
- Autophagy and apoptosis cascade: which is more prominent in neuronal death?Cellular and molecular life sciences : CMLS · 2021Review
- Alzheimer's Disease: A Molecular View of β-Amyloid Induced Morbific Events.Biomedicines · 2021Review
- Long-term depression links amyloid-β to the pathological hyperphosphorylation of tau.Cell reports · 2021Article
- Glycogen synthase kinase-3 signaling in cellular and behavioral responses to psychostimulant drugs.Biochimica et biophysica acta. Molecular cell research · 2020Review
- Neurons derived from sporadic Alzheimer's disease iPSCs reveal elevated TAU hyperphosphorylation, increased amyloid levels, and GSK3B activation.Alzheimer's research & therapy · 2017Article
- The neurotoxicity of amyloid β-protein oligomers is reversible in a primary neuron model.Molecular brain · 2017Article
- RNA Interference Silencing of Glycogen Synthase Kinase 3β Inhibites Tau Phosphorylation in Mice with Alzheimer Disease.Neurochemical research · 2016Article
- Direct High Affinity Interaction between Aβ42 and GSK3α Stimulates Hyperphosphorylation of Tau. A New Molecular Link in Alzheimer's Disease?ACS chemical neuroscience · 2016Article
- The Role of 6-Gingerol on Inhibiting Amyloid β Protein-Induced Apoptosis in PC12 Cells.Rejuvenation research · 2015Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Accumulating evidence suggests that glycogen synthase kinase 3 (GSK-3) is a multifunctional kinase implicated in Alzheimer's disease (AD). However, the synaptic actions of GSK-3 in AD conditions are largely unknown. In this study, we examined the impact of GSK-3 on N-methyl-D-aspartate receptor (NMDAR) channels, the major mediator of synaptic plasticity. Application of GSK-3 inhibitors or knockdown of GSK-3 caused a significant reduction of NMDAR-mediated ionic and synaptic current in cortical neurons, whereas this effect of GSK-3 was impaired in cortical neurons treated with β-amyloid (Aβ) or from transgenic mice overexpressing mutant amyloid precursor protein. GSK-3 activity was elevated by Aβ, and GSK-3 inhibitors failed to decrease the surface expression of NMDA receptor NR1 (NR1) and NR1/postsynaptic density-95 (PSD-95) interaction in amyloid precursor protein mice, which was associated with the diminished GSK-3 regulation of Rab5 activity that mediates NMDAR internalization. Consequently, GSK-3 inhibitor lost the capability of protecting neurons against N-methyl-D-aspartate-induced excitotoxicity in Aβ-treated neurons. These results have provided a novel mechanism underlying the involvement of GSK-3 in AD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.