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Title: Glycogen synthase kinase-3 regulates production of amyloid-β peptides and tau phosphorylation in diabetic rat brain. Author: Qu ZS, Li L, Sun XJ, Zhao YW, Zhang J, Geng Z, Fu JL, Ren QG. Journal: ScientificWorldJournal; 2014; 2014():878123. PubMed ID: 24983010. Abstract: The pathogenesis of diabetic neurological complications is not fully understood. Diabetes mellitus (DM) and Alzheimer's disease (AD) are characterized by amyloid deposits. Glycogen synthase kinase-3 (GSK-3) plays an important role in the pathogenesis of AD and DM. Here we tried to investigate the production of amyloid-β peptides (A β) and phosphorylation of microtubule-associated protein tau in DM rats and elucidate the role of GSK-3 and Akt (protein kinase B, PKB) in these processes. Streptozotocin injection-induced DM rats displayed an increased GSK-3 activity, decreased activity and expression of Akt. And A β 40 and A β 42 were found overproduced and the microtubule-associated protein tau was hyperphosphorylated in the hippocampus. Furthermore, selective inhibition of GSK-3 by lithium could attenuate the conditions of A β overproduction and tau hyperphosphorylation. Taken together, our studies suggest that GSK-3 regulates both the production of A β and the phosphorylation of tau in rat brain and may therefore contribute to DM caused AD-like neurological defects.[Abstract] [Full Text] [Related] [New Search]