ArticleFrontiers in neuroscience2016
Resveratrol Attenuates Formaldehyde Induced Hyperphosphorylation of Tau Protein and Cytotoxicity in N2a Cells.
Article in Frontiers in neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 2 of them syntheses that pooled it.
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Who cites it
44 citing papers in PubMed, 2 syntheses or guidelines pooled it, 93 citations in OpenAlex.
- Targeting Protein Aggregates with Natural Products: An Optional Strategy for Neurodegenerative Diseases.International journal of molecular sciences · 2023Pooled it
- Natural Compounds for Alzheimer's Disease Therapy: A Systematic Review of Preclinical and Clinical Studies.International journal of molecular sciences · 2019Pooled it
- Study on the improvement effect and mechanism of resveratrol on cognitive impairment in tau mutant adenovirus-induced alzheimer's disease model mice.Psychopharmacology · 2026Article
- Chronic methanol exposure induces cognitive impairment and Alzheimer's-like pathology in rhesus monkeys.Animal models and experimental medicine · 2026Article
- Formaldehyde induces and promotes Alzheimer's disease pathologies in a 3D human neural cell culture model.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2025Article
- Polyphenols and Exercise in Mitochondrial Biogenesis: Focus on Age-Related CNS Disorders.Molecular neurobiology · 2025Review
- The Multi-Dimensional Action Map of Resveratrol Against Alzheimer's Disease: Mechanism Integration and Treatment Strategy Optimization.Nutrients · 2025Review
- Resveratrol as a Therapeutic Agent in Alzheimer's Disease: Evidence from Clinical Studies.Nutrients · 2025Review
- Potential Applications of Natural Components of Traditional Chinese Medicine Delivery via Nanoparticle Drug Delivery Systems in the Treatment of Alzheimer's Disease.International journal of nanomedicine · 2025Review
- Exploring the protective effect and molecular mechanism of betulin in Alzheimer's disease based on network pharmacology, molecular docking and experimental validation.Molecular medicine reports · 2024Article
- The Potential Effects of Red Wine and Its Components on Neurocognitive Disorders: A Narrative Review.Nutrients · 2024Review
- Exogenous and endogenous formaldehyde-induced DNA damage in the aging brain: mechanisms and implications for brain diseases.Cell biology and toxicology · 2024Review
- Mechanisms of Phytoremediation by Resveratrol against Cadmium Toxicity.Antioxidants (Basel, Switzerland) · 2024Review
- Modulation of Tau Pathology in Alzheimer's Disease by Dietary Bioactive Compounds.International journal of molecular sciences · 2024Review
- Natural Compounds as Inhibitors of Aβ Peptide and Tau Aggregation.CNS & neurological disorders drug targets · 2024Review
- Resveratrol: Protective Agent Against Alzheimer's Disease.Central nervous system agents in medicinal chemistry · 2024Review
- Polyphenols and Their Impact on the Prevention of Neurodegenerative Diseases and Development.Nutrients · 2023Review
- The Protective Effect of Mangiferin on Formaldehyde-Induced HT22 Cell Damage and Cognitive Impairment.Pharmaceutics · 2023Article
- Brain targeting based nanocarriers loaded with resveratrol in Alzheimer's disease: A review.IET nanobiotechnology · 2023Review
- New Insights into Alzheimer's Disease: Novel Pathogenesis, Drug Target and Delivery.Pharmaceutics · 2023Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies have demonstrated that formaldehyde (FA)-induced neurotoxicity is important in the pathogenesis of Alzheimer's disease (AD). Elevated levels of FA have been associated with memory impairments and the main hallmarks of AD pathology, including β-amyloid plaques, tau protein hyperphosphorylation, and neuronal loss. Resveratrol (Res), as a polyphenol anti-oxidant, has been considered to have therapeutic potential for the treatment of AD. However, it has not been elucidated whether Res can exert its neuroprotective effects against FA-induced neuronal damages related to AD pathology. To answer this question, the effects of Res were investigated on Neuro-2a (N2a) cells prior to and after FA exposure. The experiments found that pre-treatment with Res significantly decreased FA-induced cytotoxicity, reduced cell apoptosis rates, and inhibited the hyperphosphorylation of tau protein at Thr181 in a dose-dependent manner. Further tests revealed that this effect was associated with the suppression of glycogen synthase kinase (GSK-3β) and calmodulin-dependent protein kinase II (CaMKII) activities, both of which are important kinases for tau protein hyperphosphorylation. In addition, Res was found to increase the activity of phosphoseryl/phosphothreonyl protein phosphatase-2A (PP2A). In summary, these findings provide evidence that Res protects N2a cells from FA-induced damages and suggests that inhibition of GSK-3β and CaMKII and the activation of PP2A by Res protect against the hyperphosphorylation and/or mediates the dephosphorylation of tau protein, respectively. These possible mechanisms underlying the neuroprotective effects of Res against FA-induced damages provide another perspective on AD treatment via inhibition of tau protein hyperhosphorylation.
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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.