ArticleNeurotoxicity research2010
Valproic acid is neuroprotective in the rotenone rat model of Parkinson's disease: involvement of alpha-synuclein.
Article in Neurotoxicity research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 1 of them a synthesis that pooled it.
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Who cites it
86 citing papers in PubMed, 1 synthesis or guideline pooled it, 176 citations in OpenAlex.
- The Role of DNA Methylation and Histone Modifications in Neurodegenerative Diseases: A Systematic Review.PloS one · 2016Pooled it
- Stress, mood, and Parkinson's disease: selective dysregulation of corticotropin-releasing hormone and urocortin neurocircuits.GeroScience · 2026Article
- Imaging brain class I histone deacetylase changes in the Lewy body dementias and Parkinson's disease.Clinical epigenetics · 2026Article
- Navigating the Autophagy Maze: ATG and Their Impact on Neurodegenerative Diseases.Molecular neurobiology · 2025Review
- Article
- Nonapoptotic role of EGL-1 in exopher production and neuronal health inProceedings of the National Academy of Sciences of the United States of America · 2025Article
- The Promise of Epigenetic Editing for Treating Brain Disorders.Sub-cellular biochemistry · 2025Review
- Protein modification in neurodegenerative diseases.MedComm · 2024Review
- Nuclear alpha-synuclein accelerates cell senescence and neurodegeneration.Immunity & ageing : I & A · 2024Article
- Non-apoptotic role of EGL-1 in exopher production and neuronal health inbioRxiv : the preprint server for biology · 2024Article
- Role of GABA pathway in motor and non-motor symptoms in Parkinson's disease: a bidirectional circuit.European journal of medical research · 2024Review
- Unlocking the epigenetic symphony: histone acetylation's impact on neurobehavioral change in neurodegenerative disorders.Epigenomics · 2024Review
- Selection of suitable reference genes for gene expression studies in HMC3 cell line by quantitative real-time RT-PCR.Scientific reports · 2024Article
- Neuroprotective Properties of Antiepileptics: What are the Implications for Psychiatric Disorders?Current medicinal chemistry · 2024Review
- Rosinidin inhibits NF-κB/ Nrf2/caspase-3 expression and restores neurotransmitter levels in rotenone-activated Parkinson's disease.Saudi journal of biological sciences · 2023Article
- Inhibition of Human Coronaviruses by Combinations of Host-Targeted and Direct-Acting Antivirals.Antimicrobial agents and chemotherapy · 2023Article
- Article
- A comprehensive review on pharmacological applications and drug-induced toxicity of valproic acid.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2023Review
- Assessing the Neurotoxicity of a Sub-Optimal Dose of Rotenone in Zebrafish (Antioxidants (Basel, Switzerland) · 2022Article
- Assessing Anti-Social and Aggressive Behavior in a Zebrafish (Brain sciences · 2022Article
26 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Valproic acid (VPA), an established antiepileptic and antimanic drug, has recently emerged as a promising neuroprotective agent. Among its many cellular targets, VPA has been recently demonstrated to be an effective inhibitor of histone deacetylases. Accordingly, we have adopted a schedule of dietary administration (2% VPA added to the chow) that results in a significant inhibition of histone deacetylase activity and in an increase of histone H3 acetylation in brain tissues of 4 weeks-treated rats. We have tested this schedule of VPA treatment in an animal model of Parkinson's disease (PD), in which degeneration of nigro-striatal dopaminergic neurons is obtained through sub-chronic administration of the mitochondrial toxin, rotenone, via osmotic mini pumps implanted to rats. The decrease of the dopaminergic marker tyrosine hydroxylase in substantia nigra and striatum caused by 7 days toxin administration was prevented in VPA-fed rats. VPA treatment also significantly counteracted the death of nigral neurons and the 50% drop of striatal dopamine levels caused by rotenone administration. The PD-marker protein alpha-synuclein decreased, in its native form, in substantia nigra and striatum of rotenone-treated rats, while monoubiquitinated alpha-synuclein increased in the same regions. VPA treatment counteracted both these alpha-synuclein alterations. Furthermore, monoubiquitinated alpha-synuclein increased its localization in nuclei isolated from substantia nigra of rotenone-treated rats, an effect also prevented by VPA treatment. Nuclear localization of alpha-synuclein has been recently described in some models of PD and its neurodegenerative effect has been ascribed to histone acetylation inhibition. Thus, the ability of VPA to increase histone acetylation is a novel candidate mechanism for its neuroprotective action.
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