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Therapeutics based on mitochondrial dysfunction and oxidative stress, such as mitochondria-targeted antioxidant [10-(4,5-dimethoxy-2-methyl-3,6-dioxo-1,4-cyclohexadien-1-yl)decyl]triphenylphosphonium methanesulfonate (MitoQ), modify disease progression by slowing the decline of mitochondrial function and disease progression in the SOD1 G93A mouse model of ALS (Miquel et al., 2014)

Further, GSH transferase which is involved in drug detoxification through conjugation of xenobiotics with GSH exhibits polymorphic forms which affect its detoxification efficacy

Quantification of the relative abundance of bacteria from the phylum Bacteroidetes in eight stool-derived communities after 48 h treatment with 10 M saxagliptin or 10 M sitagliptin in BHI or mGAM (mean SEM

The differential responses to lithium may be partially explained by TPH2 (tryptophan hydroxylase 2) whose expression is known to be downregulated by lithium [79]