Does vascular pathology contribute to Alzheimer changes?
Does vascular pathology contribute to Alzheimer changes?
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DOI：
10.1016/j.jns.2012.07.032
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发表时间：
2012-11-15
影响因子：
4.4
通讯作者：
Ihara, Masafumi
中科院分区：
文献类型：
--
作者：
Kalaria, Raj N.;Akinyemi, Rufus;Ihara, Masafumi
近年来，人们越来越关注血管疾病是否会导致阿尔茨海默病（AD）。本文综述了可改变的危险因素，如高血压，动脉粥样硬化，糖尿病，血脂异常和肥胖可能会影响血管结构和功能，促进神经退行性过程和煽动AD。动脉硬化、血管内皮细胞变性、血脑屏障功能障碍等血管病变导致慢性脑灌注不足。人脑和动物研究中的病理学变化表明脑灌注不足，这反过来又诱导AD病理学的几个特征，包括选择性脑萎缩、白色物质变化和异常蛋白如淀粉样蛋白β的积累。载脂蛋白E β 4等位基因等遗传因素可进一步修饰脑病理改变。尽管tau蛋白过度磷酸化和缠结形成仍然需要强有力的解释，但改善血管功能的干预措施减弱AD病理的证据进一步支持了血管病理影响AD变化的观点。(c)2012爱思唯尔有限公司版权所有。
In recent years there has been increased interest in whether vascular disease contributes to Alzheimer's disease (AD). This review considers how modifiable risk factors such as hypertension, atherosclerosis, diabetes, dyslipidaemia and adiposity may impact on vascular structure and function to promote neurodegenerative processes and instigate AD. The presence of vascular pathology involving arterial stiffness, arteriolosclerosis, endothelial degeneration and blood brain barrier dysfunction leads to chronic cerebral hypoperfusion. Pathological changes in human brain and animal studies suggest cerebral hypoperfusion which in turn induces several features of AD pathology including selective brain atrophy, white matter changes and accumulation of abnormal proteins such as amyloid beta. Cerebral pathological changes may be further modified by genetic factors such as the apoliopoprotein E epsilon 4 allele. Although tau hyperphosphorylation and tangle formation still needs robust explanation further support for the notion that vascular pathology influences AD changes is provided by the evidence that interventions which improve vascular function attenuate AD pathology. (c) 2012 Elsevier B.V. All rights reserved.