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Therefore, it would be crucial to understand and outline the specific contribution of each cell type MN, glia, or others to ALS, in order to strategically target them with the NRF2 activators, thereby restoring neuronal homeostasis and survival, and functional MN-glia interactions (Fig

However, in the presence of a mitochondrial glutathione the aconitase enzyme is compromised because of faulty Fe-S cluster positioning (see image below)

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Steullet P, Cabungcal JH, Kulak A, Cuenod M, Schenk F, Do KQ Glutathione deficit in animal models of schizophrenia
