PubMed: 24183963

Title
Glucagon-like peptide-1 protects hippocampal neurons against advanced glycation end product-induced tau hyperphosphorylation.
Journal
Neuroscience
Volume
256
Issue
None
Pages
137-46
Date
2014-01-03
Authors
An FM | Chen S | Gao XD | Liu AR | Yao WB | Yin DK | Yin L

Evidence 5c62c48b63

Recently, Li et al. (2012b) have demonstrated in their study that AGEs can induce tau hyperphosphorylation through receptor for advanced glycation end product (RAGE)-mediated glycogen synthase kinase 3 (GSK-3) activation and targeting RAGE/GSK-3 pathway can improve AD-like changes.

Evidence 50054d9eb1

Primary hippocampal neuron cells at different concentrations (0, 50, 100, 200 lg/ml) of glucose–BSA were incubated together for 24 h, and then thr205- phosphorylated tau was estimated by the western immunoblotting method. Western blot analysis of each experimental group showed that glucose–BSA promoted tau thr205-phosphorylation in a concentration-dependent manner (Fig. 3(a)). In the present study, it was also shown that 100 nM GLP-1 or Ex-4 treatment reduced tau hyperphosphorylation induced by glucose–BSA (Fig. 3(b, c)).

Evidence def5a078f8

Western blot analysis of different experimental groups, primary hippocampal neuron cells concurrent treatment with different concentrations (0, 50, 100, 200 lg/ml) of glucose–BSA for 24 h, also showed that glucose–BSA inhibited the phosphorylation of GSK-3b in a concentration-dependent manner (Fig. 4(a)). And 100 nM GLP-1 or Ex-4 can up-regulate phosphorylation of GSK-3b at Ser9, which was decreased by treatment with glucose–BSA (Fig. 4(b, c)).

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