Helicobacter pylori, periodontal pathogens, and their interactive association with incident all-cause and Alzheimer's disease dementia in a large national survey
Helicobacter pylori, periodontal pathogens, and their interactive association with incident all-cause and Alzheimer's disease dementia in a large national survey
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DOI：
10.1038/s41380-020-0736-2
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发表时间：
2020-05-04
影响因子：
11
通讯作者：
Zonderman, Alan B.
中科院分区：
文献类型：
--
作者：
Beydoun, May A.;Beydoun, Hind A.;Zonderman, Alan B.
幽门螺杆菌（Helicobacter pylori，Hp）与牙周致病菌的共感染可能改变阿尔茨海默病（Alzheimer's disease，AD）和全因痴呆的发病。我们在老年人（基线年龄>= 65岁）中研究了Hp血清阳性、牙周病（Pd）和感染与AD和全因痴呆的相互关系。来自国家健康和营养调查III（1988-1991）第1阶段的多达1431名参与者具有截至2014年1月1日的Hp血清阳性的完整数据，平均随访10-11年AD和全因痴呆发病率。暴露包括19种牙周病原体、构建因子和簇，以及两种Pd标记物-探测深度和临床附着丧失（CAL）。采用考克斯比例风险模型。所选样本中约55%为Hp（+）。我们发现，中间普雷沃氏菌，弯曲杆菌直，因子2（Pi/黑普雷沃氏菌/产黑色素普雷沃氏菌），和橙红色簇协同互动与Hp血清阳性，特别是关于AD发病率。较高水平的内氏放线菌（An）的存在增强了Hp（+）对AD和全因痴呆发病率的影响。相比之下，具核梭杆菌（Fn）和因子1（其中包括Fn），表现出与Hp的拮抗相互作用与全因痴呆。在Hp（+）患者中，探测深度和CAL均与全因痴呆直接相关，尽管相互作用不显著。选定的牙周病原体滴度，因素和集群相互作用大多协同，Hp血清阳性，改变AD和全因痴呆的风险。最终，需要一个随机对照试验，检查共同根除Hp和选择牙周病原体对神经退行性疾病的影响。
Co-infection between Helicobacter pylori (Hp) and groups of periodontal pathogens may alter the onset of Alzheimer's disease (AD) and all-cause dementia. We examined the interactive associations among Hp sero-positivity, periodontal disease (Pd), and infections with incident AD and all-cause dementia, among older adults (>= 65 years at baseline). Up to 1431 participants from phase 1 of the National Health and Nutrition Survey III (1988-1991) had complete data till January 1st, 2014 on Hp sero-positivity with a mean follow-up of 10-11 years for AD and all-cause dementia incidence. Exposures consisted of 19 periodontal pathogens, constructed factors and clusters, and two Pd markers- probing depth and clinical attachment loss (CAL). Cox proportional hazards models were performed. Around 55% of the selected sample was Hp(+). We found that Prevotella intermedia, Campylobacter Rectus, Factor 2 (Pi/Prevotella nigrescens/Prevotella melaninogenica), and the Orange-Red cluster interacted synergistically with Hp sero-positivity, particularly with respect to AD incidence. The presence of higher levels of Actinomyces Naeslundii (An) enhanced the effect of being Hp(+) on both AD and all-cause dementia incidence. In contrast, Fusobacterim nucleatum (Fn), and Factor 1 (which included Fn), exhibited an antagonistic interaction with Hp in relation to all-cause dementia. Both probing depth and CAL had direct associations with all-cause dementia among Hp(+) individuals, despite nonsignificant interaction. Selected periodontal pathogen titers, factors, and clusters interacted mostly synergistically, with Hp sero-positivity, to alter the risk of AD and all-cause dementia. Ultimately, a randomized controlled trial is needed, examining effects of co-eradication of Hp and select periodontal pathogens on neurodegenerative disease.