Expression of Nucleotide-binding Oligomerization Domain Receptor Protein 3 in Patients with Alzheimer's Disease and Vascular Dementia and Related Factors
10.3969/j.issn.1006-9771.2016.03.015
- VernacularTitle:核苷酸结合寡聚化结构域样受体蛋白3在阿尔茨海默病和血管性痴呆患者中的表达及相关因素研究
- Author:
Hua BAI
;
Bo YANG
;
Dejun YU
;
Qifang ZHANG
- Publication Type:Journal Article
- Keywords:
Alzheimer's disease;
vascular dementia;
nucleotide-binding oligomerization domain receptor protein 3;
inflammation;
pathogenesis
- From:
Chinese Journal of Rehabilitation Theory and Practice
2016;22(3):306-309
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the role of nucleotide-binding oligomerization domain receptor protein 3 (NLRP3) inflammasome in the pathogenesis of dementia. Methods 16 patients with with Alzheimer's disease (AD), 22 patients with vascular dementia (VD) and 20 healthy persons with similar age were detected the level of NLRP3 mRNA with RT-PCR in peripheral blood mononuclear cells January, 2014 to October, 2015. The serum level of interleukin (IL)-1βand IL-18 were detected with ELISA. The total number of white blood cells (WBC) and serum total calcium were collected. Single factor correlation analysis was performed between NLRP3mRNA and IL-1β, or IL-18, or WBC, or calcium concentration. Results The levels of NLRP3 mRNA ranged from high to low were as in AD group>VD group>the healthy group (q>11.48, P<0.05). The serum level of IL-1βwas higher in AD group than in the the healthy group (q=16.74, P<0.05), but not significantly different between VD group and the healthy group, nor between VD group and AD group (P<0.05). There was no signifi-cant difference about IL-18 among AD group, VD group and the healthy group (P<0.05). NLRP3 mRNA was positively correlated with the serum levels of IL-1β(r=0.64) and calcium (r=0.58) in AD group. There was no correlation between NLRP3 mRNA and IL-18 or WBC (P<0.05). Conclusion The expression of NLRP3 inflammasome may be related with the pathogenesis of AD, but little impact on the pathogene-sis of VD.
