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• W2808766563 abstract "Dominant mutations in an antioxidant enzyme superoxide dismutase-1 (SOD1) cause amyotrophic lateral sclerosis (ALS), an adult-onset neurodegenerative disease characterized by loss of motor neurons. Oxidative stress has also been linked to many of the neurodegenerative diseases and is likely a central mechanism of motor neuron death in ALS. Astrocytes derived from mutant SOD1G93A mouse models or patients play a significant role in the degeneration of spinal motor neurons in ALS through a non-cell-autonomous process. Here we characterize the neuroprotective effects and mechanisms of urate (a.k.a. uric acid), a major endogenous antioxidant and a biomarker of favorable ALS progression rates, in a cellular model of ALS. Our results demonstrate a significant protective effect of urate against motor neuron injury evoked by mutant astrocytes derived from SOD1G93A mice or hydrogen peroxide induced oxidative stress. Overall, these results implicate astrocyte dependent protective effect of urate in a cellular model of ALS. These findings together with our biomarker data may advance novel targets for treating motor neuron disease." @default.
• W2808766563 created "2018-06-29" @default.
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• W2808766563 date "2018-10-01" @default.
• W2808766563 modified "2023-09-26" @default.
• W2808766563 title "Urate mitigates oxidative stress and motor neuron toxicity of astrocytes derived from ALS-linked SOD1 mutant mice" @default.
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• W2808766563 doi "https://doi.org/10.1016/j.mcn.2018.06.002" @default.
• W2808766563 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29928993" @default.
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