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This document is a correction notice for an article titled "The Omega-3 Fatty Acid Eicosapentaenoic Acid Accelerates Disease Progression in a Model of Amyotrophic Lateral Sclerosis." The correction states that there are errors in the numerical values presented in Table 1 and provides the correct table. The table shows that mice administered with either a single bolus dose of EPA or fed with an EPA enriched diet had higher levels of EPA and DHA in their plasma compared to mice fed on the control diet. The correction also mentions an error in the second sentence of the first paragraph of the "Increased plasma EPA content after oral gavage or dietary supplementation with EPA" subsection of the Results, providing the correct sentence. The authors of the article are listed as Ping K. Yip, Chiara Pizzasegola, Stacy Gladman, Maria Luigia Biggio, Marianna Marino, Maduka Jayasinghe, Farhan Ullah, Simon C. Dyall, Andrea Malaspina, Caterina Bendotti, and Adina Michael-Titus. [Extracted from the article]

Amyotrophic lateral sclerosis (ALS) is a progressive fatal neurodegenerative disease characterised by loss of motor neurons that currently has no cure. Omega-3 polyunsaturated fatty acids, such as eicosapentaenoic acid (EPA), have many health benefits including neuroprotective and myoprotective potential. We tested the hypothesis that a high level of dietary EPA could exert beneficial effects in ALS. The dietary exposure to EPA (300 mg/kg/day) in a well-established mouse model of ALS expressing the G93A superoxide dismutase 1 (SOD1) mutation was initiated at a pre-symptomatic or symptomatic stage, and the disease progression was monitored until the end stage. Daily dietary EPA exposure initiated at the disease onset did not significantly alter disease presentation and progression. In contrast, EPA treatment initiated at the pre-symptomatic stage induced a significantly shorter lifespan. In a separate group of animals sacrificed before the end stage, the tissue analysis showed that the vacuolisation detected in G93A-SOD1 mice was significantly increased by exposure to EPA. Although EPA did not alter motor neurone loss, EPA reversed the significant increase in activated microglia and the astrocytic activation seen in G93A-SOD1 mice. The microglia in the spinal cord of G93A-SOD1 mice treated with EPA showed a significant increase in 4-hydroxy-2-hexenal, a highly toxic aldehydic oxidation product of omega-3 fatty acids. These data show that dietary EPA supplementation in ALS has the potential to worsen the condition and accelerate the disease progression. This suggests that great caution should be exerted when considering dietary omega-3 fatty acid supplements in ALS patients. [ABSTRACT FROM AUTHOR]