PDF(Pubmed)
Abstract：
UNASSIGNED: Observational studies have indicated the association of alteration of adipokines with Alzheimer\'s disease (AD). However, it remains unclear whether the associations are causal.
UNASSIGNED: To determine the causal associations between adipokines and AD.
UNASSIGNED: A Mendelian randomization (MR) method was applied to investigate the causal relationships of adipokines, including adiponectin and resistin, with risk of AD. Genetic proxies from genome-wide association studies (GWAS) of adiponectin and resistin were selected as instrumental variables. GWAS summary statistics for AD were extracted as outcome.
UNASSIGNED: In this study, we found evidence of the causal effects of adiponectin on AD (OR: 0.850, 95% CI: 0.731-0.990, p = 0.037). However, no relationship between resistin and AD (OR: 0.936, 95% CI: 0.851-1.029, p = 0.171) was detected. In the reverse causation analysis, null associations of AD were found for adiponectin and resistin (all p > 0.05).
UNASSIGNED: This study provides evidence of causality between adiponectin and risk of AD. However, no genetic susceptibility of resistin was discovered for AD.
UNASSIGNED: To determine the causal associations between adipokines and AD.
UNASSIGNED: A Mendelian randomization (MR) method was applied to investigate the causal relationships of adipokines, including adiponectin and resistin, with risk of AD. Genetic proxies from genome-wide association studies (GWAS) of adiponectin and resistin were selected as instrumental variables. GWAS summary statistics for AD were extracted as outcome.
UNASSIGNED: In this study, we found evidence of the causal effects of adiponectin on AD (OR: 0.850, 95% CI: 0.731-0.990, p = 0.037). However, no relationship between resistin and AD (OR: 0.936, 95% CI: 0.851-1.029, p = 0.171) was detected. In the reverse causation analysis, null associations of AD were found for adiponectin and resistin (all p > 0.05).
UNASSIGNED: This study provides evidence of causality between adiponectin and risk of AD. However, no genetic susceptibility of resistin was discovered for AD.
摘要：
■观察性研究表明脂肪因子的改变与阿尔茨海默病（AD）有关。然而,目前尚不清楚这些关联是否是因果关系.
■确定脂肪因子与AD之间的因果关系。
■应用孟德尔随机化（MR）方法研究脂肪因子的因果关系，包括脂联素和抵抗素,有AD的风险。选择脂联素和抵抗素的全基因组关联研究（GWAS）的遗传代理作为工具变量。提取AD的GWAS汇总统计数据作为结果。
■在这项研究中，我们发现了脂联素对AD的因果效应的证据(OR:0.850,95%CI:0.731-0.990,p=0.037).然而,未检测到抵抗素与AD之间的关系（OR：0.936，95％CI：0.851-1.029，p=0.171）。在反向因果关系分析中，脂联素和抵抗素与AD的相关性均为零（均p>0.05）。
■这项研究提供了脂联素与AD风险之间因果关系的证据。然而,没有发现抵抗素对AD的遗传易感性。
■确定脂肪因子与AD之间的因果关系。
■应用孟德尔随机化（MR）方法研究脂肪因子的因果关系，包括脂联素和抵抗素,有AD的风险。选择脂联素和抵抗素的全基因组关联研究（GWAS）的遗传代理作为工具变量。提取AD的GWAS汇总统计数据作为结果。
■在这项研究中，我们发现了脂联素对AD的因果效应的证据(OR:0.850,95%CI:0.731-0.990,p=0.037).然而,未检测到抵抗素与AD之间的关系（OR：0.936，95％CI：0.851-1.029，p=0.171）。在反向因果关系分析中，脂联素和抵抗素与AD的相关性均为零（均p>0.05）。
■这项研究提供了脂联素与AD风险之间因果关系的证据。然而,没有发现抵抗素对AD的遗传易感性。
