Also, the occurrence of lower GSSG and P-p38 levels and higher expression of glutamylcysteinyl ligase and glutathione peroxidase in young healthy individuals at risk of Alzheimer's disease [20] and the enhancing of the neurodegenerative phenotype in cellular and Drosophila models for Huntington's disease by treatment with N-acetyl-L-cysteine and overexpression of SOD1 support a relevant role for reductive stress in these neurodegenerative disorders [21]. The gene discussed is SOD1; the disease is Alzheimer disease.