ReviewNutrients2017
Resveratrol as a Natural Autophagy Regulator for Prevention and Treatment of Alzheimer's Disease.
Review in Nutrients, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
80 citing papers in PubMed, 1 synthesis or guideline pooled it, 145 citations in OpenAlex.
- Effects of Resveratrol Supplementation on the Cognitive Function of Patients with Alzheimer's Disease: A Systematic Review of Randomized Controlled Trials.Drugs & aging · 2022Pooled it
- Resveratrol adjunct to methylphenidate improves symptoms of attention-deficit/hyperactivity disorder: a randomized, double-blinded, placebo-controlled clinical trial.European child & adolescent psychiatry · 2021Trial
- Autophagy and selective autophagy receptors: Key players against Alzheimer's disease.Neural regeneration research · 2026Article
- Pharmacological evolution of natural product-based and chemically engineered autophagy-modulating strategies in neurodegenerative diseases: a bibliometric mapping analysis (2006-2025).Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Differential regulation of autophagy and metabolic pathways by dietary methionine and lysine deficiency in goats.BMC veterinary research · 2026Article
- Mechanistic advances in exercise‑mediated regulation of autophagy dysfunction in Alzheimer's disease (Review).International journal of molecular medicine · 2026Review
- Autophagy Modulation in Cancer Immunotherapy, Emerging Molecular Targets and Drug Selection Strategies.International journal of molecular sciences · 2026Review
- Targeting Autophagy, Ferroptosis, and Neuroinflammation: Polyphenol-Mediated Modulation of Emerging Signaling Pathways in Neurodegeneration.Molecular neurobiology · 2026Review
- Arzanol: A Review of Chemical Properties and Biological Activities.Plants (Basel, Switzerland) · 2025Review
- Resveratrol Analogs Ameliorate Mitochondrial Impairment and Insulin Resistance in a Streptozotocin-Induced In Vitro Model of Alzheimer's Disease.International journal of molecular sciences · 2025Article
- Autophagic degradation of SQSTM1 enables fibroblast activation to accelerate wound healing.Autophagy · 2025Article
- Heavy metal-induced disruption of the autophagy-lysosomal pathway: implications for aging and neurodegenerative disorders.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2025Review
- Polydatin attenuates Alzheimer's disease induced by aluminum chloride in rats: evidence for its antioxidant and anti-inflammatory effects.Frontiers in pharmacology · 2025Article
- Nutritional strategies against dementia in rural populations.Frontiers in nutrition · 2025Review
- Flavonoids and phenolic compounds: a promising avenue for neurodegenerative disease therapy.Turkish journal of biology = Turk biyoloji dergisi · 2025Review
- Regulation of aging-related chronic diseases by dietary polyphenols: An updated overview.Current research in food science · 2025Review
- Unveiling the therapeutic potential of natural products in Alzheimer's disease: insights fromFrontiers in pharmacology · 2025Review
- New Insights into the Development of Donepezil-Based Hybrid and Natural Molecules as Multi-Target Drug Agents for Alzheimer's Disease Treatment.Molecules (Basel, Switzerland) · 2024Review
- Epigenetic Explorations of Neurological Disorders, the Identification Methods, and Therapeutic Avenues.International journal of molecular sciences · 2024Review
- Protective and Detoxifying Effects of Resveratrol on Zearalenone-Mediated Toxicity: A Review.International journal of molecular sciences · 2024Review
20 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is one of the most common neurodegenerative disorders over the age of 65 years old. Although several underlying mechanisms for explaining the pathogenesis of AD are elucidated, the effective supplements or drugs for the intervention of AD are still limited. Recently, impaired autophagy associated with miRNA dysfunction has been reported to involve in aging and aging-related neurodegenerative diseases. Thus, the activation of autophagy through effectively regulating miRNAs may become a potential target for the prevention or treatment of AD. Mounting evidence from in vitro and in vivo AD models has demonstrated that resveratrol, one of polyphenolic compounds, can exert neuroprotective role in neurodegenerative diseases especially AD. In this review, the regulation of miRNAs and autophagy using resveratrol during the prevention and treatment of AD are systematically discussed, which will be beneficial to establish a target for the direct link between pharmacological intervention and AD in the future.
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What OpenQuestion holds
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.