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Benedict, C., Brooks, S.J., Kullberg, J., Burgos, J., Kempton, M.J., Nordenskjold, R., Nylander, R., Kilander, L., Craft, S., Larsson, E.-M., Johansson, L., Ahlström, H., Lind, L. and Schiöth, H.B. (2012) Impaired Insulin Sensitivity as Indexed by the HOMA Score Is Associated with Deficits in Verbal Fluency and Temporal Lobe Gray Matter Volume in the Elderly. Diabetes Care, 35, 488-494.
https://doi.org/10.2337/dc11-2075

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• TITLE: Role of GSK3β and PP2A on Regulation of Tau Phosphorylation in Hippocampus and Memory Impairment in ICV-STZ Animal Model of Alzheimer’s Disease

  AUTHORS: Teresa Ponce-Lopez, Enrique Hong, Manuel Abascal-Díaz, Alfredo Meneses

  KEYWORDS: Memory Deficit, Tau Hyperphosphorylation, GSK3β, PP2A, Streptozotocin, Hippocampus

  JOURNAL NAME: Advances in Alzheimer's Disease, Vol.6 No.1, March 10, 2017

  ABSTRACT: Intracerebroventricular administration (ICV) of streptozotocin (STZ) in rats has been associated to desensitization of the insulin receptor (IR) and biochemical changes similar to those occurring in Alzheimer’s disease (AD) or older brains, so it has been proposed as a suitable model for studying some of the pathological features of AD sporadic type (SAD). In this study, we investigated the role of glycogen synthase kinase 3β (GSK3β) and protein phosphatase 2A (PP2A) in the regulation of the phosphorylation of tau (p-tau). Results showed that ICV-STZ treated rats had deficits in short- (1.5-h) and long-term (24- and 48-h) memory after one month of ICV-STZ treatment and six months relative to control rats. The memory deficit was associated to increasing [F(3, 12) = 31.48, p β (p-GSK3β) and PP2A in hippocampus and PFC, indicating that GSK3β and PP2A contributed to regulation of p-tau. These data supporting the model with ICV-STZ in rat are adequate to study the progressive memory impairment associated to hyperphosphorylation of tau and the cascade of insulin receptor signaling; confirm that phosphatidyl-inositol-3 kinase-protein kinase B (PI3K-PKB/Akt-GSK3β) and PP2A are involved in the modulation of proteins responsible for the regulation of neurodegeneration in AD.