ArticleNeurotoxicity research2020
Tannic Acid Ameliorates STZ-Induced Alzheimer's Disease-Like Impairment of Memory, Neuroinflammation, Neuronal Death and Modulates Akt Expression.
Article in Neurotoxicity research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 53 citations in OpenAlex.
- Tannic acid attenuates glyphosate-based herbicide-induced dopaminergic neurotoxicity associated with motor dysfunction in mice.Frontiers in behavioral neuroscience · 2026Article
- Investigating the neuroprotective effects ofHeliyon · 2025Article
- Flavonoids as Natural Anti-Inflammatory Agents in the Atopic Dermatitis Treatment.Pharmaceutics · 2025Review
- Lithium Chloride Improves Electrophysiological and Memory Deficits in Rats with Streptozotocin-Induced Alzheimer's Disease.Current Alzheimer research · 2025Article
- Neuroprotective Effect of Chlorogenic Acid in an Animal Model of Sporadic Alzheimer's Disease Induced by Streptozotocin.Molecular neurobiology · 2025Article
- Aqueous extract of Spirulina exerts neuroprotection in an experimental model of Alzheimer sporadic disease in mice induced by Streptozotocin.Metabolic brain disease · 2024Article
- The Potential Effects of Red Wine and Its Components on Neurocognitive Disorders: A Narrative Review.Nutrients · 2024Review
- High-tannin food enhances spatial memory and scatter-hoarding in rodents via the microbiota-gut-brain axis.Microbiome · 2024Article
- Exendin-4 Prevents Memory Loss and Neuronal Death in Rats with Sporadic Alzheimer-Like Disease.Molecular neurobiology · 2024Article
- Tannic acid ameliorates the hazards effect of beryllium induced neuro-alterations and oxidative stress in adult male rats.Toxicology research · 2024Article
- Natural Phenolic Compounds with Neuroprotective Effects.Neurochemical research · 2024Review
- Nanoencapsulated Curcumin: Enhanced Efficacy in Reversing Memory Loss in An Alzheimer Disease Model.Brain sciences · 2024Article
- Maternal n-7 Unsaturated Fatty Acids Protect the Fetal Brain from Neuronal Degeneration in an Intrauterine Hyperglycemic Animal Model.Nutrients · 2023Article
- Ultrasmall iron-gallic acid coordination polymer nanodots with antioxidative neuroprotection for PET/MR imaging-guided ischemia stroke therapy.Exploration (Beijing, China) · 2023Article
- Non-Enzymatic Antioxidants against Alzheimer's Disease: Prevention, Diagnosis and Therapy.Antioxidants (Basel, Switzerland) · 2023Review
- Functionalized Noble Metal Nanoparticles for the Treatment of Herpesvirus Infection.Microorganisms · 2022Review
- Andrographolide Attenuates Short-Term Spatial and Recognition Memory Impairment and Neuroinflammation Induced by a Streptozotocin Rat Model of Alzheimer's Disease.Neurotoxicity research · 2022Article
- LPS-induced impairment of NaMetabolic brain disease · 2022Article
- Tannic Acid Attenuates Peripheral and Brain Changes in a Preclinical Rat Model of Glioblastoma by Modulating Oxidative Stress and Purinergic Signaling.Neurochemical research · 2022Article
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Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tannic acid (TA) is a hydrolysable glycosidic polyphenol polymer of gallic acid, which possesses neuroprotective properties. The aim of this study was to evaluate the effect of TA treatment on cognitive performance and neurochemical changes in an experimental model of sporadic dementia of Alzheimer's type (SDAT) induced by intracerebroventricular (ICV) injection of streptozotocin (STZ) and to explore the potential cellular and molecular mechanisms underlying these effects. Adult male rats were divided into four groups: control, TA, STZ, and TA + STZ. Animals from TA and TA + STZ groups were treated with TA (30 mg/kg) daily, by gavage, for 21 days; others groups received water (1 mL/kg). Subsequently, an ICV injection of STZ (3 mg/kg) was administered into the lateral ventricles of animals from STZ and TA + STZ groups, while other groups received citrate buffer. Cognitive deficits (short-term memory), neuronal survival, neuroinflammation as well as expression of SNAP-25, Akt, and pAkt were evaluated in the cerebral cortex. TA treatment protected against the impairment of memory in STZ-induced SDAT. STZ promoted an increase in neuronal death and the levels of proinflammatory cytokines (IL-6 and TNF-α) and a decrease in Akt and pAkt expression; TA was able to restore these changes. Neither STZ nor TA altered SNAP-25 expression or the levels of IL-12 and IL-4 in the cerebral cortex. Our study highlights that treatment with TA prevents memory deficits and reestablishes Akt and pAkt expression, protecting against neuronal death and neuroinflammation in STZ-induced SDAT in rats.
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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 Socratic graph.