ArticleNeural plasticity2016
Astaxanthin Protects Primary Hippocampal Neurons against Noxious Effects of Aβ-Oligomers.
Article in Neural plasticity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 65 citations in OpenAlex.
- Food-grade nanostructured delivery systems for oral administration of astaxanthin: Bioprocessing strategies and therapeutic applications.NPJ science of food · 2025Review
- Elucidation of the Neuroprotective Effects of Astaxanthin Against Amyloid β Toxicity in the SH-SY5Y Human Neuroblastoma Cell Line.Molecules (Basel, Switzerland) · 2025Article
- Review
- Pterostilbene: A natural neuroprotective stilbene with anti-Alzheimer's disease properties.Journal of pharmaceutical analysis · 2025Review
- Seaweeds as Source of Bioactive Pigments with Neuroprotective and/or Anti-Neurodegenerative Activities: Astaxanthin and Fucoxanthin.Marine drugs · 2024Review
- Amyloid β-Oligomers Inhibit the Nuclear CaAntioxidants (Basel, Switzerland) · 2023Article
- Improving the Treatment Effect of Carotenoids on Alzheimer's Disease through Various Nano-Delivery Systems.International journal of molecular sciences · 2023Review
- Combined Donepezil with Astaxanthin via Nanostructured Lipid Carriers Effective Delivery to Brain for Alzheimer's Disease in Rat Model.International journal of nanomedicine · 2023Article
- Astaxanthin Protection against Neuronal Excitotoxicity via Glutamate Receptor Inhibition and Improvement of Mitochondrial Function.Marine drugs · 2022Article
- Nanotechnology-Abetted Astaxanthin Formulations in Multimodel Therapeutic and Biomedical Applications.Journal of medicinal chemistry · 2022Review
- Recent Advancements and Future Perspectives of Microalgae-Derived Pharmaceuticals.Marine drugs · 2021Review
- Chronic Stress and Oxidative Stress as Common Factors of the Pathogenesis of Depression and Alzheimer's Disease: The Role of Antioxidants in Prevention and Treatment.Antioxidants (Basel, Switzerland) · 2021Review
- Therapeutic potential of astaxanthin and superoxide dismutase in Alzheimer's disease.Open biology · 2021Review
- Potential Therapeutic Role of Phytochemicals to Mitigate Mitochondrial Dysfunctions in Alzheimer's Disease.Antioxidants (Basel, Switzerland) · 2020Review
- Astaxanthin Counteracts Excitotoxicity and Reduces the Ensuing Increases in Calcium Levels and Mitochondrial Reactive Oxygen Species Generation.Marine drugs · 2020Article
- Role of antioxidants and a nutrient rich diet in Alzheimer's disease.Open biology · 2020Review
- Mitochondrial Dysfunctions: A Red Thread across Neurodegenerative Diseases.International journal of molecular sciences · 2020Review
- Calcium-Involved Action of Phytochemicals: Carotenoids and Monoterpenes in the Brain.International journal of molecular sciences · 2020Review
- Alzheimer's Disease-Like Pathology Triggered byFrontiers in immunology · 2020Article
- Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increased reactive oxygen species (ROS) generation and the ensuing oxidative stress contribute to Alzheimer's disease pathology. We reported previously that amyloid-β peptide oligomers (AβOs) produce aberrant Ca(2+) signals at sublethal concentrations and decrease the expression of type-2 ryanodine receptors (RyR2), which are crucial for hippocampal synaptic plasticity and memory. Here, we investigated whether the antioxidant agent astaxanthin (ATX) protects neurons from AβOs-induced excessive mitochondrial ROS generation, NFATc4 activation, and RyR2 mRNA downregulation. To determine mitochondrial H2O2 production or NFATc4 nuclear translocation, neurons were transfected with plasmids coding for HyperMito or NFATc4-eGFP, respectively. Primary hippocampal cultures were incubated with 0.1 μM ATX for 1.5 h prior to AβOs addition (500 nM). We found that incubation with ATX (≤10 μM) for ≤24 h was nontoxic to neurons, evaluated by the live/dead assay. Preincubation with 0.1 μM ATX also prevented the neuronal mitochondrial H2O2 generation induced within minutes of AβOs addition. Longer exposures to AβOs (6 h) promoted NFATc4-eGFP nuclear translocation and decreased RyR2 mRNA levels, evaluated by detection of the eGFP-tagged fluorescent plasmid and qPCR, respectively. Preincubation with 0.1 μM ATX prevented both effects. These results indicate that ATX protects neurons from the noxious effects of AβOs on mitochondrial ROS production, NFATc4 activation, and RyR2 gene expression downregulation.
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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.