Linking cardiometabolic disorders to sporadic Alzheimer's disease: a perspective on potential mechanisms and mediators.
Linking cardiometabolic disorders to sporadic Alzheimer's disease: a perspective on potential mechanisms and mediators.
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DOI：
10.1111/j.1471-4159.2010.06978.x
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发表时间：
2010-11
影响因子：
4.7
通讯作者：
Bhat NR
中科院分区：
文献类型：
--
作者：
Bhat NR
越来越多的证据表明，阿尔茨海默病（AD）的发病率受到心血管危险因素的显著影响，这些危险因素与包括糖尿病和动脉粥样硬化在内的一系列代谢性疾病相关。共同的风险也反映在饮食和生活方式与代谢紊乱和AD型认知功能障碍的联系中。最近对遗传和饮食诱导的动物模型的研究已经开始阐明这两类具有不同组织特异性病理的疾病状况之间的会聚机制和介质。虽然外周炎症和胰岛素抵抗是代谢综合征疾病发病机制的核心，但似乎相同的机制也在血脑屏障（BBB）中发挥作用，导致AD样分子和认知变化。本次审查将突出这些收敛机制，并讨论脑血管功能障碍的作用，作为一个管道，以大脑出现的这些致病过程，也可能代表未来的治疗目标，在AD中常见的代谢紊乱。
There is increasing evidence that the incidence of Alzheimer's disease (AD) is significantly influenced by cardiovascular risk factors in association with a cluster of metabolic diseases including diabetes and atherosclerosis. The shared risk is also reflected in the dietary and lifestyle links to both metabolic disorders and AD-type cognitive dysfunction. Recent studies with genetic and diet-induced animal models have begun to illuminate convergent mechanisms and mediators between these two categories of disease conditions with distinct tissue-specific pathologies. While it is clear that peripheral inflammation and insulin resistance are central to the pathogenesis of the disorders of metabolic syndrome, it seems that the same mechanisms are also in play across the blood brain barrier (BBB) that lead to AD-like molecular and cognitive changes. This review will highlight these convergent mechanisms and discuss the role of cerebrovascular dysfunction as a conduit to brain emergence of these pathogenic processes that might also represent future therapeutic targets in AD in common with metabolic disorders.
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