Alzheimer's Silent Partner: Cerebral Amyloid Angiopathy
Alzheimer's Silent Partner: Cerebral Amyloid Angiopathy
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DOI：
10.1007/s12975-013-0309-7
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发表时间：
2014-06-01
影响因子：
6.9
通讯作者：
Zabel, Matthew K.
中科院分区：
文献类型：
--
作者：
Cupino, Tanya L.;Zabel, Matthew K.
阿尔茨海默病（AD）是最常见的痴呆症，完全缺乏可行的长期治疗干预。这部分是由于对AD病因学以及与其基因型和表型异质性相关的可能混杂因素的不完全理解。脑淀粉样血管病（CAA）是一种常见的，但经常被忽视，病理与AD。CAA表现为脑动脉和小动脉的平滑肌层内淀粉样蛋白-β（A β）的沉积。A β在AD和CAA病理生理学中的作用长期以来一直存在争议。尽管它在体外已被证明具有超生理水平的毒性，但A β负荷并不一定与人类的认知死亡相关。本文就CAA在AD病理生理中的作用以及可能导致血管脆性和血管扩张的重要病理机制作一综述。此外，我们讨论了A β对平滑肌细胞表型和活力的影响，特别是在补体级联方面。
Alzheimer's disease (AD) is the most common form of dementia, which completely lacks a viable, long-term therapeutic intervention. This is partly due to an incomplete understanding of AD etiology and the possible confounding factors associated with its genotypic and phenotypic heterogeneity. Cerebral amyloid angiopathy (CAA) is a common, yet frequently overlooked, pathology associated with AD. CAA manifests with deposition amyloid-beta (A beta) within the smooth muscle layer of cerebral arteries and arterioles. The role of A beta in AD and CAA pathophysiology has long been controversial. Although it has demonstrated toxicity at super-physiological levels in vitro, A beta load does not necessarily correlate with cognitive demise in humans. In this review, we describe the contributions of CAA to AD pathophysiology and important pathomechanisms that may lead to vascular fragility and hemorrhages. Additionally, we discuss the effect of A beta on smooth muscle cell phenotype and viability, especially in terms of the complement cascade.