Research on glycogen synthase kinase-3β and hyperphosphorylation of tau protein in rats combined type 2 diabetes and Alzheimer's disease
10.3760/cma.j.issn.0254-9026.2010.01.021
- VernacularTitle:2型糖尿病及阿尔茨海默病大鼠糖原合成酶-3β和tau蛋白磷酸化的研究
- Author:
Yi ZHANG
;
Shenglin ZHANG
;
Fenghua GAG
;
Yun CHEN
;
Xiaojuan YANG
- Publication Type:Journal Article
- Keywords:
Diabetes mellitus;
type 2;
Alzheimer disease;
Glycogen synthase kinase 3;
Oxidative plosphorylation
- From:
Chinese Journal of Geriatrics
2010;29(1):63-66
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the possible pathogenesis of type 2 diabetes mellitus (T2DM) combined with Alzheimer's disease (AD). Methods Wistar rats were randomly divided into control, T2DM, AD and T2DM +AD groups. The blood glucose levels were assayed, and the behavior changes were tested by Morris water maze. The glycogen synthase kinase-3β (GSK-3β) and hyperphosphorylation of tau protein were detected by immunohistochemistry staining. Results Compared with the control rats, the learning and memory abilities were weakened significantly in the model rats (F=28. 65, P<0.001). The expression of GSK-3β was higher in T2DM + AD group (4319. 02±653. 24) than in AD group (304. 39 ± 175. 83), T2DM group (540.43 ± 558.49) and control group (315. 56 ± 91. 64, H=19. 335, all P<0. 01). The level of hyperphosphorylation of tau protein was significantly increased in T2DM + AD group (8583. 81 ± 2236. 11) and AD group (2799. 61±1070. 02) than in control group (252. 02 ± 58. 37) and T2DM group (287. 75 ± 192. 53, H=32. 950, P< 0.001). There was no significantly difference of hyperphosphorylation of tau between T2DM group and control group (H = 32. 950, P>0. 05). Conclusions The increasing of GSK-3β activity in T2DM may be caused by hyperphosphorylation of tau.
