Findings from Tianjin Medical University Update Knowledge of Type 2 Diabetes (Folic Acid Reduces Tau Phosphorylation by Regulating PP2A Methylation in Streptozotocin-Induced Diabetic Mice)
By a News Reporter-Staff News Editor at Diabetes Week -- Data detailed on Nutritional and Metabolic Diseases and Conditions - Type 2 Diabetes have been presented. According to news reporting from Tianjin, People's Republic of China, by NewsRx journalists, research stated, "High incidence rate of Alzheimer's disease (AD) is observed in patients with type 2 diabetes. Aggregated beta-amyloid (A beta) and hyperphosphorylated tau are the hallmarks of AD."
The news correspondents obtained a quote from the research from Tianjin Medical University, "Hyperphosphorylated tau has been detected in diabetic animals as well as in diabetic patients. Folates mediate the transfer of one carbon unit, required in various biochemical reactions. The effect of folate on tau phosphorylation in diabetic models still remains unknown. In this study, we investigated the effect and mechanism of folic acid on hyperphosphorylation of tau in streptozotocin (STZ)-induced diabetic mice. Diabetic mice induced by STZ, at the age of 10 weeks, were administered with three levels of folic acid: folic acid-deficient diet, diet with normal folic acid content, and 120 mu g/kg folic acid diet for 8 weeks. Levels of serum folate and blood glucose were monitored. Tau phosphorylation, protein phosphatase 2A (PP2A) methylation, and Glycogen synthase kinase 3 beta (GSK-3 beta) phosphorylation were detected using Western blot. The S-adenosyl methionine: S-adenosyl homocysteine ratio (SAM:SAH) in brain tissues was also determined. DNA methyltransferase (DNMT) mRNA expression levels were detected using real-time PCR. Folic acid reduced tau hyperphosphorylation at Ser396 in the brain of diabetes mellitus (DM) mice. In addition, PP2A methylation and DNMT1 mRNA expression were significantly increased in DM mice post folic acid treatment. GSK-3 beta phosphorylation was not regulated by folic acid administration. Folic acid can reduce tau phosphorylation by regulating PP2A methylation in diabetic mice."
According to the news reporters, the research concluded: "These results support that folic acid can serve as a multitarget neuronal therapeutic agent for treating diabetes-associated cognitive dysfunction."
For more information on this research see: Folic Acid Reduces Tau Phosphorylation by Regulating PP2A Methylation in Streptozotocin-Induced Diabetic Mice. International Journal of Molecular Sciences, 2017;18(4):3019-3031. International Journal of Molecular Sciences can be contacted at: Mdpi Ag, St Alban-Anlage 66, Ch-4052 Basel, Switzerland (see also Nutritional and Metabolic Diseases and Conditions - Type 2 Diabetes).
Our news journalists report that additional information may be obtained by contacting M.Y. Zheng, Tianjin Med Univ, Tianjin Inst Endocrinol, Tianjin 300070, People's Republic of China. Additional authors for this research include C. Zou, M.Y. Li, G.W. Huang, Y.X. Gao and H. Liu.
Keywords for this news article include: Tianjin, People's Republic of China, Asia, Nutritional and Metabolic Diseases and Conditions, Neurodegenerative Diseases and Conditions, Non-Insulin Dependent Diabetes Mellitus, Risk and Prevention, Alzheimer Disease, Pharmaceuticals, Type 2 Diabetes, Endocrinology, Folic Acid, Genetics, Tianjin Medical University.
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