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阿尔茨海默病与:探索联系。 你提供的原文似乎不完整,“and”后面缺少内容。

Alzheimer's Disease and : Exploring the Links.

作者信息

Shawkatova Ivana, Durmanova Vladimira, Javor Juraj

机构信息

Institute of Immunology, Faculty of Medicine, Comenius University in Bratislava, Odborarske nam. 14, 811 08 Bratislava, Slovakia.

出版信息

Life (Basel). 2025 Jan 14;15(1):96. doi: 10.3390/life15010096.

Abstract

Recent research highlights compelling links between oral health, particularly periodontitis, and systemic diseases, including Alzheimer's disease (AD). Although the biological mechanisms underlying these associations remain unclear, the role of periodontal pathogens, particularly , has garnered significant attention. , a major driver of periodontitis, is recognized for its potential systemic effects and its putative role in AD pathogenesis. This review examines evidence connecting to hallmark AD features, such as amyloid β accumulation, tau hyperphosphorylation, neuroinflammation, and other neuropathological features consistent with AD. Virulence factors, such as gingipains and lipopolysaccharides, were shown to be implicated in blood-brain barrier disruption, neuroinflammation, and neuronal damage. -derived outer membrane vesicles may serve to disseminate virulence factors to brain tissues. Indirect mechanisms, including systemic inflammation triggered by chronic periodontal infections, are also supposed to exacerbate neurodegenerative processes. While the exact pathways remain uncertain, studies detecting virulence factors and its other components in AD-affected brains support their possible role in disease pathogenesis. This review underscores the need for further investigation into -mediated mechanisms and their interplay with host responses. Understanding these interactions could provide critical insights into novel strategies for reducing AD risk through periodontal disease management.

摘要

最近的研究突出了口腔健康,尤其是牙周炎,与包括阿尔茨海默病(AD)在内的全身性疾病之间存在令人信服的联系。尽管这些关联背后的生物学机制尚不清楚,但牙周病原体的作用,尤其是[此处原文缺失具体病原体名称],已引起了广泛关注。[此处原文缺失具体病原体名称]作为牙周炎的主要驱动因素,因其潜在的全身影响及其在AD发病机制中的假定作用而受到认可。本综述探讨了将[此处原文缺失具体病原体名称]与AD标志性特征联系起来的证据,如淀粉样β蛋白积累、tau蛋白过度磷酸化、神经炎症以及与AD一致的其他神经病理学特征。毒力因子,如牙龈蛋白酶和脂多糖被证明与血脑屏障破坏、神经炎症和神经元损伤有关。[此处原文缺失具体病原体名称]衍生的外膜囊泡可能有助于将毒力因子传播到脑组织。间接机制,包括慢性牙周感染引发的全身炎症,也被认为会加剧神经退行性过程。虽然确切途径仍不确定,但在受AD影响的大脑中检测到[此处原文缺失具体病原体名称]毒力因子及其其他成分的研究支持了它们在疾病发病机制中的可能作用。本综述强调需要进一步研究[此处原文缺失具体病原体名称]介导的机制及其与宿主反应的相互作用。了解这些相互作用可能为通过牙周疾病管理降低AD风险的新策略提供关键见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94a5/11766648/e852fc375e4a/life-15-00096-g001.jpg

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