While prevailing evidence supports that the amyloid cascade hypothesis is a key component of Alzheimer’s disease (AD) pathology, many recent studies indicate that the vascular system is also a major contributor to disease progression. Vascular dysfunction and reduced cerebral blood flow (CBF) occurprior to the accumulation and aggregation of amyloid-β (Aβ) plaques and hyperphosphorylated tau tangles. Although research has predominantly focused on the cellular processes involved with Aβ-mediated neurodegeneration, effects of Aβ on CBF and neurovascular coupling are becoming more evident. This review will describe AD vascular disturbances as they relate to Aβ, including chronic cerebral hypoperfusion, hypertension, altered neurovascular coupling, and deterioration of the blood-brain barrier. In addition, we will describe recent findings about the relationship between these vascular defects and Aβ accumulation with emphasis on in vivo studies utilizing rodent AD models.

中文翻译：

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阿尔茨海默氏病：β-淀粉样蛋白与神经血管功能障碍之间的联系

虽然流行的证据支持淀粉样蛋白级联假说是阿尔茨海默氏病（AD）病理的关键组成部分，但许多最新研究表明，血管系统也是疾病进展的主要因素。血管功能障碍和脑血流量减少（CBF）发生在淀粉样β（Aβ）斑块和过度磷酸化的tau缠结的积累和聚集之前。尽管研究主要集中在与Aβ介导的神经变性有关的细胞过程中，但Aβ对CBF和神经血管偶联的作用变得越来越明显。这篇综述将描述与Aβ相关的AD血管疾病，包括慢性脑灌注不足，高血压，神经血管耦合改变和血脑屏障恶化。此外，