ArticleEuropean journal of nutrition2016
Resveratrol reduces amyloid-beta (Aβ₁₋₄₂)-induced paralysis through targeting proteostasis in an Alzheimer model of Caenorhabditis elegans.
Article in European journal of nutrition, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 2 of them syntheses that pooled it.
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Who cites it
70 citing papers in PubMed, 2 syntheses or guidelines pooled it, 147 citations in OpenAlex.
- Neuroprotective Effects of Resveratrol in In vivo and In vitro Experimental Models of Parkinson's Disease: a Systematic Review.Neurotoxicity research · 2022Pooled it
- The proteasome as a druggable target with multiple therapeutic potentialities: Cutting and non-cutting edges.Pharmacology & therapeutics · 2020Pooled it
- Do Grape- and Wine-Derived (Poly)Phenols Contribute to the Hallmarks of Healthy Brain Ageing?Nutrients · 2026Review
- A Purified Lycii Fructus Polysaccharide Fraction Extends Healthspan inAntioxidants (Basel, Switzerland) · 2026Article
- Matrix and intermembrane space-specific mitochondrial stress response in Alzheimer's disease.NPJ dementia · 2026Article
- The Role of Plant-Derived Bioactive Compounds in Mitigating Oxidative Stress.Foods (Basel, Switzerland) · 2025Review
- Stilbenes Against Alzheimer's Disease: A Comprehensive Review of Preclinical Studies of Natural and Synthetic Compounds Combined with the Contributions of Developed Nanodrug Delivery Systems.Molecules (Basel, Switzerland) · 2025Review
- A Brief Review on Caenorhabditis elegans Role in Modelling Neurodegenerative Disease.Central nervous system agents in medicinal chemistry · 2025Review
- Natural autophagy modulators in non-communicable diseases: from autophagy mechanisms to therapeutic potential.Acta pharmacologica Sinica · 2025Review
- Naturido alleviates amyloid β1-42-induced adverse effects in a transgenic Caenorhabditis elegans model of Alzheimer's disease.PloS one · 2025Article
- Selective protein degradation through chaperone‑mediated autophagy: Implications for cellular homeostasis and disease (Review).Molecular medicine reports · 2025Review
- Mechanism and Clinical Application Prospects of Mitochondrial DNA Single Nucleotide Polymorphism in Neurodegenerative Diseases.Neurochemical research · 2024Review
- Exploring the Neuroprotective Effects of Grape Seed Procyanidins on Amyloid-β-Induced Toxicity inFoods (Basel, Switzerland) · 2024Article
- Resveratrol protects pancreatic beta cell and hippocampal cells from the aggregate-prone capacity of hIAPP.Scientific reports · 2024Article
- The Potential Effects of Red Wine and Its Components on Neurocognitive Disorders: A Narrative Review.Nutrients · 2024Review
- Silver nanoparticles alter the dimerization of AβRSC advances · 2024Article
- Review Deciphering the Anticancer Efficacy of Resveratrol and their Associated Mechanisms in Human Carcinoma.Endocrine, metabolic & immune disorders drug targets · 2024Review
- Investigating hormesis, aging, and neurodegeneration: From bench to clinics.Open medicine (Warsaw, Poland) · 2024Review
- Mitochondrial Quality Control via Mitochondrial Unfolded Protein Response (mtUPR) in Ageing and Neurodegenerative Diseases.Biomolecules · 2023Review
- Abl depletion via autophagy mediates the beneficial effects of quercetin against Alzheimer pathology across species.Cell death discovery · 2023Article
10 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeResveratrol is a polyphenol present in red wine for which the capability of directly interfering with the hallmark of Alzheimer's disease (AD), i.e. toxic β-amyloid protein (Aβ) aggregation, has been shown recently. Since the stimulation of proteostasis could explain reduced Aβ-aggregation, we searched for proteostasis targets of resveratrol.
methodsThe transgenic Caenorhabditis elegans strain CL2006, expressing Aβ1-42 under control of a muscle-specific promoter and responding to Aβ-toxicity with paralysis, was used as a model. Target identification was accomplished through specific knockdowns of proteostasis genes by RNA interference. Effects of resveratrol on protein aggregation were identified using ProteoStat(®) Detection Reagent, and activation of proteasomal degradation by resveratrol was finally proven using a specific fluorogenic peptide substrate.
resultsResveratrol at a concentration of 100 µM caused a 40 % decrease in paralysis. UBL-5 involved in unfolded protein response (UPR) in mitochondria proved to be necessary for the prevention of Aβ-toxicity by resveratrol. Also XBP-1, which represents an endoplasmic reticulum-resident factor involved in UPR, was identified to be necessary for the effects of resveratrol. Regarding protein degradation pathways, the inhibition of macroautophagy and chaperone-mediated autophagy prevented resveratrol from reducing paralysis as did the inhibition of proteasomal degradation. Finally, resveratrol reduced the amount of lysosomes, suggesting increased flux of proteins through the autophagy pathways and activated proteasomal degradation.
conclusionsResveratrol reduces the Aβ-induced toxicity in a C. elegans model of AD by targeting specific proteins involved in proteostasis and thereby reduces the amount of aggregated Aβ.
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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.