[Age-dependent expression of HSP90 in the hippocampus of APP/PS1 mice].

The present study aims to observe the change in expression of heat shock protein 90 (HSP90) along with amyloid-β (Aβ) and phosphorylated Tau (p-Tau) protein levels in the hippocampus tissue of Alzheimer's disease (AD) transgenic animal model with age. APP/PS1 transgenic mice at age of 6-, 9- and 12-month and C57BL/6J mice of the same age were used. The cognitive abilities of these animals were evaluated using a Morris water maze.

[Time dependent expression profiling of PTK2B and its relationship with Aβ, Tau and LRP-1 in hippocampus and blood of APPswe/PS1dE9 double-transgenic mouse].

To uncover the time-dependent expression pattern of gene and encoded protein, protein tyrosine kinase 2 beta(PTK2B), in the brain tissues of transgenic animal models of Alzheimer's disease (AD) and its relationship with the levels of Aβ phosphorylation of Tau (p-Tau) and low density lipoprotein receptor-related protein-1(LRP-1) in blood and brain tissues. In this study, 5-, 10- and 15-month-old APPswe/PS1dE9 double-transgenic mice harboring the genotype of AD confirmed by the gene test were divided into the 5-, 10- and 15-month-old experiment groups, and simultaneously, age-matched C57BL/6J mice were placed into the corresponding control groups, with 8 mice in each group. All mice were subjected to the Morris Water Maze for test of cognitive and behavioral ability.

[PTK2B affects the levels of Aβ in blood and brain and behavioral functions via targeting LRP-1 transporter in Aβ-induced cognitive dysfunction mice].

The aim of the present study was to explore the correlation between ptk2b/PTK2B (protein tyrosine kinase 2 beta, a ptk2b-encoded protein) and the level of low density lipoprotein receptor-related protein-1 (LRP-1), as well as to uncover the relationship between the changes in beta amyloid protein (Aβ) levels in blood and brain and the expression of ptk2b in Aβ-induced cognitive dysfunction mice. A total of 64 3-month-old C57BL/6J mice were divided randomly into the experimental group and control group. All mice underwent the intracerebroventricular (i.

Histone deacetylase-6 modulates amyloid beta-induced cognitive dysfunction rats by regulating PTK2B.

The aim of this study was to investigate the effects of histone deacetylase-6 (HDAC6) on the functional and pathological changes of the amyloid beta (Aβ)-induced cognitive dysfunction rats by regulating protein tyrosine kinase 2 beta (PTK2B). Ninety Sprague Dawley rats were randomly divided into nine groups, consisting of five experimental groups and four control groups. In five experimental groups, Aβ1-42 was infused intracerebroventricularly and 3 days later, rats in each group were infused intracerebroventricularly with tubastatin A hydrochloride (TSA), the HDAC6-specific inhibitor (Aβ + TSA group), theophylline, the HDACs agonist (Aβ + Theo group), PF431396 (PF), the PTK2B inhibitor (Aβ + PF group), the combination of PF and theophylline (Aβ + PF + Theo group), and normal saline (Aβ + normal saline group), respectively.

Histone deacetyltase 6 modulates amyloid β-induced cognitive dysfunction rats by regulating protein tyrosine kinase 2 beta.

The aim of this study was to investigate the effects of histone deacetyltase (HDAC) 6 on the functional and pathological changes of the amyloid beta (Aβ)-induced cognitive dysfunction rats by regulating protein tyrosine kinase 2 beta (PTK2B). Ninety Sprague-Dawley rats were randomly divided into nine groups, consisting of five experimental groups and four control groups. In five experimental groups, Aβ1-42 was infused intracerebroventricularly and 3 days later, rats in each group were infused intracerebroventricularly with tubastatin A hydrochloride (TSA), the histone deacetyltase 6 (HDAC6)-specific inhibitor (Aβ + TSA group), theophylline, the HDACs agonist (Aβ + theophylline group), PF431396, the PTK2B inhibitor (Aβ + PF group), the combination of PF431396 and theophylline (Aβ + PF + theophylline group) and normal saline (Aβ + normal saline group), respectively.