ArticleJournal of molecular neuroscience : MN2015
Histone deacetylase inhibitor, trichostatin A, improves learning and memory in high-fat diet-induced cognitive deficits in mice.
Article in Journal of molecular neuroscience : MN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 73 citations in OpenAlex.
- Article
- Central Role of Toll-like Receptor-9 Gene Function in Inflammation-Mediated Neuronal Plasticity: Implications for Long-Term Memory Development.Molecular neurobiology · 2025Review
- Histone Deacetylase 9 Deletion Inhibits Hepatic Steatosis and Adipose Tissue Inflammation in Male Diet-Induced Obese Mice.Journal of gastroenterology and hepatology · 2025Article
- The Promise of Epigenetic Editing for Treating Brain Disorders.Sub-cellular biochemistry · 2025Review
- HDAC3 inhibition protects against peripheral and central alterations in an animal model of obesity.Pharmacological reports : PR · 2023Article
- Brain insulin resistance linked Alzheimer's and Parkinson's disease pathology: An undying implication of epigenetic and autophagy modulation.Inflammopharmacology · 2023Review
- Alpha synuclein post translational modifications: potential targets for Parkinson's disease therapy?Frontiers in molecular neuroscience · 2023Review
- Neuroprotective Effect of Lentivirus-Mediated FGF21 Gene Delivery in Experimental Alzheimer's Disease is Augmented when Concerted with Rapamycin.Molecular neurobiology · 2022Article
- Epigenetic regulation and autophagy modulation debilitates insulin resistance associated Alzheimer's disease condition in rats.Metabolic brain disease · 2022Article
- Vorinostat Corrects Cognitive and Non-Cognitive Symptoms in a Mouse Model of Fragile X Syndrome.The international journal of neuropsychopharmacology · 2022Article
- Beneficial Effects of Exogenous Ketogenic Supplements on Aging Processes and Age-Related Neurodegenerative Diseases.Nutrients · 2021Review
- Exploring the Neuroprotective Potential of Rosiglitazone Embedded Nanocarrier System on Streptozotocin Induced Mice Model of Alzheimer's Disease.Neurotoxicity research · 2021Article
- Postnatal Ethanol Exposure Activates HDAC-Mediated Histone Deacetylation, Impairs Synaptic Plasticity Gene Expression and Behavior in Mice.The international journal of neuropsychopharmacology · 2020Article
- Action of trichostatin A on Alzheimer's disease-like pathological changes in SH-SY5Y neuroblastoma cells.Neural regeneration research · 2020Article
- Epigenetic regulation of motivated behaviors by histone deacetylase inhibitors.Neuroscience and biobehavioral reviews · 2019Review
- Preventive Effect of Two New Neurotensin Analogues on Parkinson's Disease Rat Model.Journal of molecular neuroscience : MN · 2018Article
- GABAergic inhibitory neurons as therapeutic targets for cognitive impairment in schizophrenia.Acta pharmacologica Sinica · 2018Review
- Understanding Epigenetics in the Neurodegeneration of Alzheimer's Disease: SAMP8 Mouse Model.Journal of Alzheimer's disease : JAD · 2018Review
- A Low-Cost Morris Water Maze for Undergraduate Research: Construction and Demonstration in a Rat Model of Obesity-Induced Diabetes.Journal of undergraduate neuroscience education : JUNE : a publication of FUN, Faculty for Undergraduate Neuroscience · 2018Article
- Administration of a Histone Deacetylase Inhibitor into the Basolateral Amygdala Enhances Memory Consolidation, Delays Extinction, and Increases Hippocampal BDNF Levels.Frontiers in pharmacology · 2017Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
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Abstract
Metabolic syndrome is increasingly recognized for its effects on cognitive health. Recent studies have highlighted the role of histone deacetylases (HDACs) in metabolic syndrome and cognitive functions. The present study was designed to investigate the possible therapeutic role of a HDAC inhibitor, trichostatin A (TSA), in cognitive impairment associated with metabolic syndrome. To ascertain the mechanisms involved, we fed mice with high-fat diet (HFD) for 4 weeks and examined changes in behavioral and biochemical/oxidative stress markers. Mice subjected to HFD exhibited characteristic features of metabolic disorder, viz., hyperglycemia, hypertriglyceridemia, hypercholesterolemia, and lower high-density lipoprotein (HDL) cholesterol levels. Moreover, these mice showed severe deficits in learning and memory as assessed by the Morris water maze and passive avoidance tasks along with elevated oxidative stress and inflammatory markers in brain homogenates. The observed changes occurred concurrently with reduced brain-derived neurotrophic factor (BDNF). In contrast, the mice treated with the HDAC inhibitor, TSA (0.5 and 1 mg/kg, i.p.), showed a significant and dose-dependent reduction in serum glucose, triglycerides, and total cholesterol along with improvement in HDL-cholesterol levels and learning and memory performance. TSA treatment also results in alleviation of oxidative stress and neuroinflammatory markers. Moreover, TSA significantly augmented the BDNF levels in HFD-fed mice. Thus, based upon these observations, it may be suggested that HDAC inhibition could be a novel therapeutic strategy to combat cognitive impairment associated with metabolic syndrome.
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