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Description
Within neurons, oxidative stress may stem from mitochondrial dysfunction induced by the intracellular accumulation of hyperphosphorylated tau and A [84, 120]
These responses involve the coordinated upregulation of antioxidant genes, glutathione S-transferase (GST ), catalase (Cat), glutathione-peroxidase (GPxs), hemeoxygenase1 (HO-1) and peroxiredoxins (Prdxs), to lessen the oxidative load and restore cellular homeostasis
Human cd4(+)Cd25(+) thymocytes and peripheral T cells have immune suppressive activity in vitro
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