The glyoxylate and dicarboxylate metabolic pathways ameliorated by SeM are believed to be related to mitochondrial dysfunction, and their dysfunction leads to increased Aβ production in vivo, which is consistent with our results showing increased levels of COX IV (an enzyme complex of the mitochondrial respiratory chain) and reduced Aβ production in SeM-treated AD mice. The gene discussed is COX4I1; the disease is Alzheimer disease.