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Functional reduction in SFXN4 expression led to mitochondriopathy and impaired erythropoiesis in two human subjects [49]

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In a fALS transgenic mouse model, the SOD1 G86R mouse, this drug delayed the disease onset, improved motor function, and rescued neuronal death by regulating the glycosphingolipid metabolism, a pathway that is importantly altered in the CNS of these mice and ALS patients (Dodge et al., 2015