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Mixed evidence for the relationship between periodontitis and Alzheimer's disease: A bidirectional Mendelian randomization study.
PLOS ONE ( IF 2.9 ) Pub Date : 2020-01-24 , DOI: 10.1371/journal.pone.0228206 Yi-Qian Sun 1, 2 , Rebecca C Richmond 3 , Yue Chen 4 , Xiao-Mei Mai 5
PLOS ONE ( IF 2.9 ) Pub Date : 2020-01-24 , DOI: 10.1371/journal.pone.0228206 Yi-Qian Sun 1, 2 , Rebecca C Richmond 3 , Yue Chen 4 , Xiao-Mei Mai 5
Affiliation
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Recent experimental studies indicated that a periodontitis-causing bacterium might be a causal factor for Alzheimer's disease (AD). We applied a two-sample Mendelian randomization (MR) approach to examine the potential causal relationship between chronic periodontitis and AD bidirectionally in the population of European ancestry. We used publicly available data of genome-wide association studies (GWAS) on periodontitis and AD. Five single-nucleotide polymorphisms (SNPs) were used as instrumental variables for periodontitis. For the MR analysis of periodontitis on risk of AD, the causal odds ratio (OR) and 95% confidence interval (CI) were derived from the GWAS of periodontitis (4,924 cases vs. 7,301 controls) and from the GWAS of AD (21,982 cases vs. 41,944 controls). Seven non-overlapping SNPs from another latest GWAS of periodontitis was used to validate the above association. Twenty SNPs were used as instrumental variables for AD. For the MR analysis of liability to AD on risk of periodontitis, the causal OR was derived from the GWAS of AD including 30,344 cases and 52,427 controls and from the GWAS of periodontitis consisted of 12,289 cases and 22,326 controls. We employed multiple methods of MR. Using the five SNPs as instruments of periodontitis, there was suggestive evidence of genetically predicted periodontitis being associated with a higher risk of AD (OR 1.10, 95% CI 1.02 to 1.19, P = 0.02). However, this association was not verified using the seven independent SNPs (OR 0.97, 95% CI 0.87 to 1.08, P = 0.59). There was no association of genetically predicted AD with the risk of periodontitis (OR 1.00, 95% CI 0.96 to 1.04, P = 0.85). In summary, we did not find convincing evidence to support periodontitis being a causal factor for the development of AD. There was also limited evidence to suggest genetic liability to AD being associated with the risk of periodontitis.
中文翻译：
牙周炎与阿尔茨海默氏病之间关系的混合证据：孟德尔双向随机研究。
最近的实验研究表明，引起牙周炎的细菌可能是阿尔茨海默氏病（AD）的致病因素。我们应用了两个样本的孟德尔随机（MR）方法来检查欧洲血统人群中慢性牙周炎和AD之间的潜在因果关系。我们使用了有关牙周炎和AD的全基因组关联研究（GWAS）的公开数据。五个单核苷酸多态性（SNP）被用作牙周炎的工具变量。对于牙周炎对AD风险的MR分析，因果比（OR）和95％置信区间（CI）来自牙周炎的GWAS（4,924例vs. 7,301例对照）和AD的GWAS（21,982例）对比41,944个控件）。来自另一个最新的牙周炎GWAS的7个不重叠的SNP用于验证上述关联。二十个SNP被用作AD的工具变量。为了对牙周炎风险对AD的责任进行MR分析，因果OR来自AD的GWAS，包括30,344例病例和52,427例对照，以及牙周炎的GWAS，包括12,289例病例和22,326例对照。我们采用了多种MR方法。使用这五个SNP作为牙周炎的手段，有迹象表明遗传预测的牙周炎与AD风险较高相关（OR 1.10，95％CI 1.02至1.19，P = 0.02）。但是，没有使用七个独立的SNP（OR 0.97，95％CI 0.87至1.08，P = 0.59）来验证这种关联。遗传学上预测的AD与牙周炎的风险没有关联（OR 1.00，95％CI为0.96至1.04，P = 0.85）。总而言之，我们没有发现令人信服的证据来支持牙周炎是AD发生的原因。也有有限的证据表明对AD的遗传易感性与牙周炎的风险有关。
更新日期：2020-01-26
中文翻译：
牙周炎与阿尔茨海默氏病之间关系的混合证据：孟德尔双向随机研究。
最近的实验研究表明，引起牙周炎的细菌可能是阿尔茨海默氏病（AD）的致病因素。我们应用了两个样本的孟德尔随机（MR）方法来检查欧洲血统人群中慢性牙周炎和AD之间的潜在因果关系。我们使用了有关牙周炎和AD的全基因组关联研究（GWAS）的公开数据。五个单核苷酸多态性（SNP）被用作牙周炎的工具变量。对于牙周炎对AD风险的MR分析，因果比（OR）和95％置信区间（CI）来自牙周炎的GWAS（4,924例vs. 7,301例对照）和AD的GWAS（21,982例）对比41,944个控件）。来自另一个最新的牙周炎GWAS的7个不重叠的SNP用于验证上述关联。二十个SNP被用作AD的工具变量。为了对牙周炎风险对AD的责任进行MR分析，因果OR来自AD的GWAS，包括30,344例病例和52,427例对照，以及牙周炎的GWAS，包括12,289例病例和22,326例对照。我们采用了多种MR方法。使用这五个SNP作为牙周炎的手段，有迹象表明遗传预测的牙周炎与AD风险较高相关（OR 1.10，95％CI 1.02至1.19，P = 0.02）。但是，没有使用七个独立的SNP（OR 0.97，95％CI 0.87至1.08，P = 0.59）来验证这种关联。遗传学上预测的AD与牙周炎的风险没有关联（OR 1.00，95％CI为0.96至1.04，P = 0.85）。总而言之，我们没有发现令人信服的证据来支持牙周炎是AD发生的原因。也有有限的证据表明对AD的遗传易感性与牙周炎的风险有关。
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