ArticleNeurochemical research2013
Alterations on Na⁺,K⁺-ATPase and acetylcholinesterase activities induced by amyloid-β peptide in rat brain and GM1 ganglioside neuroprotective action.
Article in Neurochemical research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 44 citations in OpenAlex.
- Mechanisms mediating effects of cardiotonic steroids in mammalian blood cells.Frontiers in pharmacology · 2025Review
- Beta-amyloid influences the content and trafficking of beta-amyloid precursor protein via Na,K-ATPase-Src kinase positive feedback loop.Frontiers in pharmacology · 2025Article
- Review
- Ganglioside GM1 and the Central Nervous System.International journal of molecular sciences · 2023Review
- Article
- Start Me Up: How Can Surrounding Gangliosides Affect Sodium-Potassium ATPase Activity and Steer towards Pathological Ion Imbalance in Neurons?Biomedicines · 2022Review
- Structure and function of glycosphingolipids on small extracellular vesicles.Glycoconjugate journal · 2022Review
- Effect of curcumin nanoparticles on streptozotocin-induced male Wistar rat model of Alzheimer's disease.Metabolic brain disease · 2022Article
- Interactions of Amyloid-β with Membrane Proteins.International journal of molecular sciences · 2021Review
- Review
- GM1 Oligosaccharide Crosses the Human Blood-Brain Barrier In Vitro by a Paracellular Route.International journal of molecular sciences · 2020Article
- Phosphorylation of the Amyloid-Beta Peptide Inhibits Zinc-Dependent Aggregation, Prevents Na,K-ATPase Inhibition, and Reduces Cerebral Plaque Deposition.Frontiers in molecular neuroscience · 2018Article
- Impact of GMBiophysical journal · 2017Review
- Enhanced Autophagy Contributes to Protective Effects of GM1 Ganglioside Against Aβ1-42-Induced Neurotoxicity and Cognitive Deficits.Neurochemical research · 2017Article
- Monosialoganglioside 1 may alleviate neurotoxicity induced by propofol combined with remifentanil in neural stem cells.Neural regeneration research · 2017Article
- Alzheimer's disease AβDoklady. Biochemistry and biophysics · 2017Article
- GM1 Ganglioside Inhibits β-Amyloid Oligomerization Induced by Sphingomyelin.Angewandte Chemie (International ed. in English) · 2016Article
- Direct interaction of beta-amyloid with Na,K-ATPase as a putative regulator of the enzyme function.Scientific reports · 2016Article
- GM1 Ganglioside: Past Studies and Future Potential.Molecular neurobiology · 2016Review
- P2C-Type ATPases and Their Regulation.Molecular neurobiology · 2016Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a neurodegenerative disorder whose pathogenesis involves production and aggregation of amyloid-β peptide (Aβ). Aβ-induced toxicity is believed to involve alterations on as Na(+),K(+)-ATPase and acetylcholinesterase (AChE) activities, prior to neuronal death. Drugs able to prevent or to reverse these biochemical changes promote neuroprotection. GM1 is a ganglioside proposed to have neuroprotective roles in AD models, through mechanisms not yet fully understood. Therefore, this study aimed to investigate the effect of Aβ1-42 infusion and GM1 treatment on recognition memory and on Na(+),K(+)-ATPase and AChE activities, as well as, on antioxidant defense in the brain cortex and the hippocampus. For these purposes, Wistar rats received i.c.v. infusion of fibrilar Aβ1-42 (2 nmol) and/or GM1 (0.30 mg/kg). Behavioral and biochemical analyses were conducted 1 month after the infusion procedures. Our results showed that GM1 treatment prevented Aβ-induced cognitive deficit, corroborating its neuroprotective function. Aβ impaired Na(+),K(+)-ATPase and increase AChE activities in hippocampus and cortex, respectively. GM1, in turn, has partially prevented Aβ-induced alteration on Na(+),K(+)-ATPase, though with no impact on AChE activity. Aβ caused a decrease in antioxidant defense, specifically in hippocampus, an effect that was prevented by GM1 treatment. GM1, both in cortex and hippocampus, was able to increase antioxidant scavenge capacity. Our results suggest that Aβ-triggered cognitive deficit involves region-specific alterations on Na(+),K(+)-ATPase and AChE activities, and that GM1 neuroprotection involves modulation of Na(+),K(+)-ATPase, maybe by its antioxidant properties. Although extrapolation from animal findings is difficult, it is conceivable that GM1 could play an important role in AD treatment.
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