ArticleJournal of molecular neuroscience : MN2013
Edaravone prevents neurotoxicity of mutant L166P DJ-1 in Parkinson's disease.
Article in Journal of molecular neuroscience : MN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Revisiting Glutamate Excitotoxicity in Amyotrophic Lateral Sclerosis and Age-Related Neurodegeneration.International journal of molecular sciences · 2024Review
- The Antioxidant Drug Edaravone Binds to the Aryl Hydrocarbon Receptor (AHR) and Promotes the Downstream Signaling Pathway Activation.Biomolecules · 2024Article
- Effects of the Edaravone, a Drug Approved for the Treatment of Amyotrophic Lateral Sclerosis, on Mitochondrial Function and Neuroprotection.Antioxidants (Basel, Switzerland) · 2022Review
- Traumatic Brain Injury: Oxidative Stress and Novel Anti-Oxidants Such as Mitoquinone and Edaravone.Antioxidants (Basel, Switzerland) · 2020Review
- Elevated expression of DJ-1 (encoded by the human PARK7 gene) protects neuronal cells from sevoflurane-induced neurotoxicity.Cell stress & chaperones · 2018Article
- Edaravone protects against hyperosmolarity-induced oxidative stress and apoptosis in primary human corneal epithelial cells.PloS one · 2017Article
- Edaravone promotes functional recovery after mechanical peripheral nerve injury.Neural regeneration research · 2014Article
- Oxygen-glucose-deprived rat primary neural cells exhibit DJ-1 translocation into healthy mitochondria: a potent stroke therapeutic target.CNS neuroscience & therapeutics · 2014Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD), which is estimated to affect approximately 1 % of the population over the age of 65, is the second most common neurodegenerative disorder after Alzheimer's disease. It was reported that pathogenic mutations in DJ-1 lead to autosomal recessive early-onset familial Parkinsonism. The L166P mutant of DJ-1 is the most commonly studied loss-of-function mutation in early onset familial PD, but the underlying mechanisms are still unknown. Edaravone is a powerful free radical scavenger used in clinical treatment for cerebral ischemic stroke. In the present study, we investigated the effects of edaravone on the neurotoxicity in PD-induced isoforms of DJ-1 containing the mutation L166P. Our results indicated that edaravone was able to significantly attenuate oxidative stress and improve mitochondrial function. Furthermore, edaravone was found to reduce apoptosis in Neuro2a cells through modulation of mitochondria-dependent apoptosis pathways. Interestingly, our result also demonstrated that edaravone was able to up-regulate VMAT2 expression in N2a cells in a dose-dependent manner. Our findings enhance the understanding of the neuro-protective effects of edaravone in cell models and suggest that edaravone offers significant protection in a PD-related in vitro model.
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