Nelson Lucy, Gard Paul, Tabet Naji
Brighton and Sussex Medical School, University of Brighton, Falmer, Brighton, UK.
School of Pharmacy and Biomolecular Sciences, University of Brighton, Brighton, East Sussex, UK.
J Alzheimers Dis. 2014;41(2):331-43. doi: 10.3233/JAD-140024.
Alzheimer's disease (AD) is by far the most common sporadic neurodegenerative disorder. Clinically it is associated with cognitive and other neuropsychological impairments, and neuropathologically it is distinguished by presence of amyloid-β plaques and neurofibrillary tangles. Hypertension has been traditionally associated with the etiology of vascular dementia, however, vascular risk factors including hypertension are increasingly being implicated in AD. Likewise, the importance of neuroinflammation in AD pathogenesis is also widely recognized. Data from animal and non-AD human studies suggest a close reciprocal relationship between hypertension and inflammatory systems. Much less is known on the potential pathological interaction between hypertension and inflammation in AD and its subsequent effects on amyloid and tau misfolding, aggregation, and propagation, events recognized as critical for the development and progression of AD. This review summarizes what is known about the mechanistic interactions between hypertension and inflammatory mediators and assesses their potential synergistic/additive role in AD genesis. Increasing our understanding of the pathological interactions between the recognized risk factors for AD is a worthwhile endeavor in a condition which currently has limited treatment options but an increasing number of potential preventative measures.
阿尔茨海默病（AD）是目前最常见的散发性神经退行性疾病。临床上，它与认知及其他神经心理障碍相关，在神经病理学上，其特征是存在β淀粉样蛋白斑块和神经原纤维缠结。传统上，高血压与血管性痴呆的病因有关，然而，包括高血压在内的血管危险因素越来越多地与AD相关。同样，神经炎症在AD发病机制中的重要性也得到了广泛认可。来自动物和非AD人类研究的数据表明，高血压与炎症系统之间存在密切的相互关系。关于高血压与炎症在AD中的潜在病理相互作用及其对淀粉样蛋白和tau蛋白错误折叠、聚集和传播的后续影响，我们所知甚少，而这些事件被认为对AD的发生和发展至关重要。本综述总结了关于高血压与炎症介质之间机制相互作用的已知信息，并评估了它们在AD发生中的潜在协同/相加作用。在目前治疗选择有限但潜在预防措施不断增加的情况下，加深我们对AD公认危险因素之间病理相互作用的理解是一项有价值的努力。
