Inhibition of amyloid-induced toxicity by ergothioneine in a transgenic Caenorhabditis elegans model
| Autor: | Vanessa Yuk Man Lam, Jan Gruber, Barry Halliwell, Keith Hsiu Chin Lim, Li Fang Ng, Li-Theng Ng, Cheryl Y.W. Huang, Irwin K. Cheah, Fang‐Qin Goh |
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| Rok vydání: | 2019 |
| Předmět: |
Amyloid
Transgene Biophysics medicine.disease_cause Biochemistry Neuroprotection Antioxidants Animals Genetically Modified 03 medical and health sciences chemistry.chemical_compound Structural Biology Genetics medicine Animals Humans Paralysis Caenorhabditis elegans Molecular Biology 030304 developmental biology 0303 health sciences Amyloid beta-Peptides biology Dose-Response Relationship Drug 030302 biochemistry & molecular biology Neurotoxicity Ergothioneine Cell Biology medicine.disease biology.organism_classification Cell biology Disease Models Animal Oxidative Stress Treatment Outcome chemistry Alzheimer's disease Oxidative stress |
| Zdroj: | FEBS lettersReferences. 593(16) |
| ISSN: | 1873-3468 |
| Popis: | The abnormal accumulation of β-amyloid peptide (Aβ) is recognized as a central component in the pathogenesis of Alzheimer disease. While many aspects of Aβ-mediated neurotoxicity remain elusive, Aβ has been associated with numerous underlying pathologies, including oxidative and nitrosative stress, inflammation, metal ion imbalance, mitochondrial dysfunction, and even tau pathology. Ergothioneine (ET), a naturally occurring thiol/thione-derivative of histidine, has demonstrated antioxidant and neuroprotective properties against various oxidative and neurotoxic stressors. This study investigates ET's potential to counteract Aβ-toxicity in transgenic Caenorhabditis elegans overexpressing a human Aβ peptide. The accumulation of Aβ in this model leads to paralysis and premature death. We show that ET dose-dependently reduces Aβ-oligomerization and extends the lifespan and healthspan of the nematodes. |
| Databáze: | OpenAIRE |
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