ArticleJournal of neurochemistry2025
Ergothioneine Treatment Ameliorates the Pathological Phenotypes of Parkinson's Disease Models.
Article in Journal of neurochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed.
- Article
- The therapeutic opportunities and pitfalls of using iron ion chelators to treat neurodegenerative diseases.FEBS letters · 2026Review
- Is Ergothioneine an Important Source of Plasma TrimethylamineAntioxidants (Basel, Switzerland) · 2026Article
- Organic cation transporter novel 1 (OCTN1): beyond an ergothioneine transporter.Cell communication and signaling : CCS · 2026Review
- Potential Protection Against Parkinson's Disease by Ergothioneine-Nature's Multifactorial Neuroprotectant.Antioxidants (Basel, Switzerland) · 2026Review
- Ergothioneine as a potential protective agent against macular degeneration and other eye disorders.Scientific reports · 2026Article
- Ketogenic diet and Parkinson's disease.Frontiers in molecular neuroscience · 2026Review
- Ergothioneine Treatment Ameliorates the Pathological Phenotypes of Parkinson's Disease Models.Journal of neurochemistry · 2025Article
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
Ergothioneine (ET) is a naturally occurring thiol/thione that possesses several cytoprotective properties. Multiple studies suggest a potential neuroprotective role for ET. Here, we show in various Parkinson's disease (PD) models that ET is indeed neuroprotective. Firstly, using Drosophila genetic PD models, we demonstrated that ET treatment ameliorates the pathological phenotypes of parkin and LRRK2 PD mutant flies. This includes an improvement in their climbing score and the preservation of their dopaminergic neuronal number and mitochondrial integrity. Similarly, we observed the rescue of PD phenotypes by ET in mice treated with the Parkinsonian neurotoxin 6-OHDA. This protective effect of ET is abolished in mice lacking OCTN1. Finally, we found that ET protects human LRRK2-G2019S patient-derived dopaminergic neurons from rotenone-induced neurotoxicity; the action of ET is again OCTN1-dependent. Collectively, our results strongly support a neuroprotective role for ET in PD and suggest that ET may be useful in the prevention and/or treatment of PD.
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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.