Department of Neurology, University of California San Francisco, 305 Parnassus Avenue, San Francisco, CA 94143, USA.
Exp Gerontol. 2012 Nov;47(11):838-42. doi: 10.1016/j.exger.2012.08.005. Epub 2012 Aug 28.
Cerebral amyloid angiopathy (CAA) is an age-associated disease characterized by amyloid deposition in cerebral and meningeal vessel walls. CAA is detected in the majority of the individuals with dementia and also in a large number of non-demented elderly individuals. In addition, CAA is strongly associated with Alzheimer's disease (AD) pathology. Mechanical consequences including intra-cerebral or subarachnoid hemorrhage remains CAA most feared complication, but only a small fraction of CAA results in severe bleeding. On the hand the non-mechanical consequences in cerebrovascular regulation are prevalent and may be even more deleterious. Studies of animal models have provided strong evidence linking the vasoactive Aβ 1-40, the main species found in CAA, to disturbances in endothelial-dependent factors, disrupting cerebrovascular regulation Here, we aimed to review experimental findings regarding the non-mechanical consequences of CAA for cerebrovascular regulation and discuss the implications of these results to clinical practice.
脑淀粉样血管病(Cerebral amyloid angiopathy,CAA)是一种与年龄相关的疾病,其特征是脑和脑膜血管壁中有淀粉样物质沉积。CAA 存在于大多数痴呆患者中,也存在于大量非痴呆老年人中。此外,CAA 与阿尔茨海默病(Alzheimer's disease,AD)病理密切相关。机械性后果,包括脑内或蛛网膜下腔出血,仍然是 CAA 最可怕的并发症,但只有一小部分 CAA 会导致严重出血。另一方面,血管调节中非机械性后果普遍存在,甚至可能更具危害性。动物模型研究提供了强有力的证据,表明在 CAA 中主要存在的血管活性 Aβ 1-40 与内皮依赖性因子的紊乱有关,从而破坏了脑血管调节。在这里,我们旨在综述有关 CAA 对脑血管调节的非机械性后果的实验研究结果,并讨论这些结果对临床实践的意义。