ArticleNeuroscience letters2013
Valproic acid ameliorates C. elegans dopaminergic neurodegeneration with implications for ERK-MAPK signaling.
Article in Neuroscience letters, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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.
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Who cites it
21 citing papers in PubMed, 25 citations in OpenAlex.
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- 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
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- Probing the importance of AIF interaction with endonuclease G in mitochondrial inheritance and neurodegeneration.Cell discovery · 2024Article
- Protein mimetic 2D FAST rescues alpha synuclein aggregation mediated early and post disease Parkinson's phenotypes.Nature communications · 2024Article
- Non-apoptotic role of EGL-1 in exopher production and neuronal health inbioRxiv : the preprint server for biology · 2024Article
- Using aPharmaceuticals (Basel, Switzerland) · 2022Article
- UsingFrontiers in pharmacology · 2022Review
- Valproic Acid Reduces Vasospasm through Modulation of Akt Phosphorylation and Attenuates Neuronal Apoptosis in Subarachnoid Hemorrhage Rats.International journal of molecular sciences · 2021Article
- Attenuation of epigenetic regulator SMARCA4 and ERK-ETS signaling suppresses aging-related dopaminergic degeneration.Aging cell · 2020Article
- Probiotic Bacillus subtilis Protects against α-Synuclein Aggregation in C. elegans.Cell reports · 2020Article
- Found in Translation: The Utility ofBrain sciences · 2019Review
- East Indian sandalwood (RSC advances · 2018Article
- Divalproex sodium modulates nuclear localization of ataxin-3 and prevents cellular toxicity caused by expanded ataxin-3.CNS neuroscience & therapeutics · 2018Article
- Modeling Parkinson's Disease in C. elegans.Journal of Parkinson's disease · 2018Review
- Behavioral Phenotyping and Pathological Indicators of Parkinson's Disease inFrontiers in genetics · 2017Review
- Six psychotropics for pre-symptomatic & early Alzheimer's (MCI), Parkinson's, and Huntington's disease modification.Neural regeneration research · 2016Review
- Using C. elegans to discover therapeutic compounds for ageing-associated neurodegenerative diseases.Chemistry Central journal · 2015Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Parkinson's disease (PD) is a currently incurable neurodegenerative disorder that affects the aging population. The loss of dopaminergic neurons in the substantia nigra is one of the pathological features of PD. The precise causes of PD remain unresolved but evidence supports both environmental and genetic contributions. Current efforts for the treatment of PD are directed toward the discovery of compounds that show promise in impeding age-dependent neurodegeneration in PD patients. Alpha-synuclein (α-Syn) is a human protein that is mutated in specific populations of patients with familial PD. Overexpression of α-Syn in animal models of PD replicates key symptoms of PD, including neurodegeneration. Here, we use the nematode Caenorhabditis elegans as a model system, whereby α-Syn toxicity causes dopaminergic neurodegeneration, to test the capacity of valproic acid (VA) to protect neurons. The results of our study showed that treatment of nematodes with moderate concentrations of VA significantly protects dopaminergic neurons against α-Syn toxicity. Consistent with previously established knowledge related to the mechanistic action of VA in the cell, we showed through genetic analysis that the neuroprotection conferred by VA is inhibited by cell-specific depletion of the C. elegans ortholog of the MAP extracellular signal-regulated kinase (ERK), MPK-1, in the dopaminergic neurons. These findings suggest that VA may exert its neuroprotective effect via ERK-MAPK, or alternately could act with MAPK signaling to additively provide dopaminergic neuroprotection.
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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 OpenQuestion graph.