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In addition, changes in the levels of proteins, such as A42, tau, and neuron-specific enolase in the serum or cerebrospinal fluid, also provide clues to the mechanism of disease-induced neurodegeneration (70, 71)

Notably, GSH binding motif is not conserved among the other seleno-GPxs (GPx2, GPx3, GPx4, and GPx6) justifying their abilities to use wide variety of thiols like cysteine, protein thiols, mercaptoethanol, and dithiothreitol in addition to GSH as reducing equivalent for the catalysis [8, 17, 18]