Changes and correlation between serum β-amyloid 1-42 and total bilirubin in patients with Alzheimer′s disease
10.3760/cma.j.cn112150-20240813-00652
- VernacularTitle:阿尔茨海默病患者血清β-淀粉样蛋白1-42与总胆红素的水平变化及相关性研究
- Author:
Xiaoyu WANG
1
;
Hu DENG
;
Wei LI
;
Yanfang ZHOU
;
Shujuan PAN
Author Information
1. 北京回龙观医院医学检验中心 北京大学回龙观临床医学院，北京 100096
- Publication Type:Journal Article
- Keywords:
Alzheimer′s disease;
Aβ accumulation;
β-amyloid 1-42;
Total bilirubin;
Antioxidants
- From:
Chinese Journal of Preventive Medicine
2024;58(12):1987-1993
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the levels of β-amyloid 1-42 (Aβ1-42) and total bilirubin (TBIL) in serum of patients with Alzheimer ′s disease (AD) and the relationship between them.Methods:A case-control study was conducted to select 73 patients with AD who were hospitalized in Beijing Huilongguan Hospital from November 2023 to February 2024 as AD group, and 70 healthy controls (HC) were selected as HC group. The basic information of all subjects and the clinical information of AD patients were collected, and the levels of Aβ1-42 and TBIL were detected and compared between the two groups. The effects of Aβ1-42 and TBIL on AD were analyzed by binary logistic regression. Correlation analysis was used to analyze the relationship between TBIL and Aβ1-42 in AD group and HC group. According to the level of Aβ1-42 in AD patients, they were divided into Aβ1-42 elevated group and Aβ1-42 normal group. The differences of clinical data and TBIL levels between the two groups were compared. According to the quartile of TBIL in AD patients, they were divided into Q1 group, Q2 group, Q3 group and Q4 group. The correlation between TBIL and the risk of Aβ1-42 elevation was analyzed by binary logistic regression. The receiver operating characteristic (ROC) curve was drawn to analyze the ability of TBIL level to predict the increase of Aβ1-42 in AD patients.Results:There was no significant difference in gender, marital status, education level, smoking and drinking between AD group and HC group ( P>0.05), while the levels of Aβ1-42 and TBIL and age in AD group were significantly higher than those in HC group [101.10(71.20, 128.60) pg/ml/22.40(10.00, 39.60) pg/ml , Z=-8.714, P<0.001;(11.00±3.22/8.07±3.00) μmol/L , t=5.621, P<0.001;(77.14±8.20/68.30±10.27) years, t=5.672, P<0.001]. For AD patients, the TBIL level in the Aβ1-42 elevated group was lower than that in the Aβ1-42 normal group [(10.05±2.94/11.66±3.28) μmol/L , t=-2.148, P=0.035], while there was no significant difference in other demographic and clinical data between the two groups ( P>0.05). Binary logistic regression analysis showed that higher levels of Aβ1-42 ( OR=1.021, 95% CI：1.010-1.032) and TBIL ( OR=1.505, 95% CI：1.249-1.814), older age ( OR=1.083, 95% CI：1.020-1.150) and female ( OR=4.348, 95% CI：1.253-15.094) were risk factors for AD. Correlation analysis showed that TBIL was negatively correlated with Aβ1-42 in AD patients ( r=-0.322, P=0.006). After adjusting the relevant covariates, binary logistic regression showed that compared with AD patients in Q1 group, the risk of Aβ1-42 elevation in AD patients in Q4 group was lower ( OR=0.052, 95% CI：0.005-0.535, P<0.05), and TBIL was negatively correlated with the risk of Aβ1-42 elevation ( P trend<0.05). ROC curve showed that the area under the curve (AUC) of TBIL in predicting the increase of Aβ1-42 in AD patients was 0.642. Conclusion:The levels of Aβ1-42 and TBIL in AD patients were higher, and the level of TBIL was negatively correlated with the risk of Aβ1-42 elevation.
