p(HGNC:GLP1R)

Entity

Name

GLP1R

Namespace

hgnc

Namespace Version

20180906

Namespace URL

https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Tau Modifications Sections of NESTOR

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)). PubMed:24183963

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)). PubMed:24183963

In this study, we demonstrated that GLP-1RA could inhibit oxidative stress and repair mitochondrial damage in addition to decreasing tau hyperphosphorylation in PC12 cells treated with AGEs. Importantly, we first observed AGEs in the circulatory system could induce tau hyperphosphorylation after we injected AGEs (1μg/kg bodyweight) into the mice tail vein. We found GLP-1RA could promote mitochondrial biogenesis and antioxidant system via regulating peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) signaling pathway in vivo besides down-regulating the activity of glycogen synthase kinase 3β (GSK-3β) to reverse tau hyperphosphorylation directly. PubMed:25987199

In this study, we demonstrated that GLP-1RA could inhibit oxidative stress and repair mitochondrial damage in addition to decreasing tau hyperphosphorylation in PC12 cells treated with AGEs. Importantly, we first observed AGEs in the circulatory system could induce tau hyperphosphorylation after we injected AGEs (1μg/kg bodyweight) into the mice tail vein. We found GLP-1RA could promote mitochondrial biogenesis and antioxidant system via regulating peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) signaling pathway in vivo besides down-regulating the activity of glycogen synthase kinase 3β (GSK-3β) to reverse tau hyperphosphorylation directly. PubMed:25987199