ArticleMolecular neurobiology2018
Histone Deacetylase 2 Inhibition Attenuates Downregulation of Hippocampal Plasticity Gene Expression during Aging.
Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 71 citations in OpenAlex.
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- The histone deacetylase family in health and disease.Signal transduction and targeted therapy · 2026Review
- Mitochondrial-Epigenetic Crosstalk in Autism Spectrum Disorder: Linking Cellular Stress to Synaptic Dysfunction and Treatment Resistance.Molecular neurobiology · 2026Review
- Histone modification dynamics in brain aging: unlocking therapeutic potential.Cell death & disease · 2026Review
- Histone Deacetylase 2 in Alzheimer's Disease: A Comprehensive Molecular Blueprint for Therapeutic Targeting.Molecular neurobiology · 2025Review
- Tripartite Interaction of Epigenetic Regulation, Brain Aging, and Neuroinflammation: Mechanistic Insights and Therapeutic Implications.Epigenomes · 2025Review
- The impact of sex on memory during aging and Alzheimer's disease progression: Epigenetic mechanisms.Journal of Alzheimer's disease : JAD · 2024Review
- TAF15 Overexpression Impairs Memory in Mice by Inhibiting the Transcription of Npas4.Neuroscience bulletin · 2024Article
- Article
- Tat-Beclin-1 Ameliorates Memory by Improving Neuronal Cytoarchitecture and Mitigating Mitochondrial Dysfunction in Scopolamine-Induced Amnesic Male Mice.ACS pharmacology & translational science · 2024Article
- Class 1 histone deacetylases differentially modulate memory and synaptic genes in a spatial and temporal manner in aged and APP/PS1 mice.Brain research · 2024Article
- Exercise epigenetics is fueled by cell bioenergetics: Supporting role on brain plasticity and cognition.Free radical biology & medicine · 2024Review
- An Overview of the Epigenetic Modifications in the Brain under Normal and Pathological Conditions.International journal of molecular sciences · 2024Review
- DNA methylation, histone acetylation in the regulation of memory and its modulation during aging.Frontiers in aging · 2024Review
- Suv39h1 Silencing Recovers Memory Decline in Scopolamine-Induced Amnesic Mouse Model.Molecular neurobiology · 2024Article
- Correlational patterns of neuronal activation and epigenetic marks in the basolateral amygdala and piriform cortex following olfactory threat conditioning and extinction in rats.Frontiers in molecular neuroscience · 2024Article
- Activation of βMolecular psychiatry · 2023Article
- Tryptophan metabolite norharman secreted by cultivated Lactobacillus attenuates acute pancreatitis as an antagonist of histone deacetylases.BMC medicine · 2023Article
- Modulation of Synaptic Plasticity Genes Associated to DNA Damage in a Model of Huntington's Disease.Neurochemical research · 2023Article
- 5-Methylcytosine and 5-Hydroxymethylcytosine in Scrapie-Infected Sheep and Mouse Brain Tissues.International journal of molecular sciences · 2023Article
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2 authors at 1 institution in 1 country.
Funding
Abstract
The brain undergoes several anatomical, biochemical, and molecular changes during aging, which subsequently result in downregulation of synaptic plasticity genes and decline of memory. However, the regulation of these genes during aging is not clearly understood. Previously, we reported that the expression of histone deacetylase (HDAC)2 was upregulated in the hippocampus of old mice and negatively correlated with the decline in recognition memory. As HDAC2 regulates key synaptic plasticity neuronal immediate early genes (IEGs), we have examined their expression and epigenetic regulation. We noted that the expression of neuronal IEGs decreased both at mRNA and protein level in the hippocampus of old mice. To explore the underlying regulation, we analyzed the binding of HDAC2 and level of histone acetylation at the promoter of neuronal IEGs. While the binding of HDAC2 was higher, H3K9 and H3K14 acetylation level was lower at the promoter of these genes in old as compared to young and adult mice. Further, we inhibited HDAC2 non-specifically by sodium butyrate and specifically by antisense oligonucleotide to recover epigenetic modification, expression of neuronal IEGs, and memory in old mice. Inhibition of HDAC2 increased histone H3K9 and H3K14 acetylation level at the promoter of neuronal IEGs, their expression, and recognition memory in old mice as compared to control. Thus, inhibition of HDAC2 can be used as a therapeutic target to recover decline in memory due to aging and associated neurological disorders.
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