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In our recent study, in addition to elucidating the pathogenic mechanism of FUS-associated ALS in both Drosophila and animal systems, we found that overexpression of GstO2, a Drosophila homolog of human GSTO1, reduces cytoplasmic FUS aggregates and attenuates neurodegenerative phenotypes, including mitochondrial dysfunction and neuronal toxicity 148

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Dietary polyunsaturated fatty acids and inflammatory mediator production

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Enhanced SIRT6 activity abrogates the neurotoxic phenotype of astrocytes expressing ALS-linked mutant SOD1