Department of Cell Biology and Anatomy, National Cheng Kung University. 1 Ta Hsueh Road, Tainan, Taiwan 70101.
Curr Alzheimer Res. 2014 Jan;11(1):4-10. doi: 10.2174/1567205010666131119234308.
Accumulation, aggregation and deposition of the amyloid-β (Aβ) peptides in the brain are widely accepted as the central events in the pathogenesis of Alzheimer's disease (AD). Any factor that is capable of causing these events is potentially a risk factor for AD. In the last decade, evidence has accumulated to support the association between cerebral vascular diseases (CVD) and AD. CVD is known to induce amyloid deposition and affects the age of onset for sporadic AD; whereas, amyloid deposition has been shown to cause cerebrovascular degeneration. In this review, we propose a positive feedback loop between CVD and amyloid deposition. The disease cycle could be triggered by aging and/or other environmental factor-associated CVD, as in late-onset sporadic AD patients, or by over production of Aβ, as in the familial AD patients and amyloid precursor protein transgenic animals.
淀粉样蛋白-β（Aβ）肽在大脑中的积累、聚集和沉积被广泛认为是阿尔茨海默病（AD）发病机制中的核心事件。任何能够导致这些事件的因素都可能是 AD 的风险因素。在过去的十年中，有证据表明脑血管疾病（CVD）与 AD 之间存在关联。已知 CVD 可诱导淀粉样蛋白沉积，并影响散发性 AD 的发病年龄；而淀粉样蛋白沉积已被证明可导致脑血管退化。在这篇综述中，我们提出了 CVD 和淀粉样蛋白沉积之间的正反馈回路。疾病周期可能由衰老和/或其他与环境因素相关的 CVD 引发，如晚发性散发性 AD 患者，或由 Aβ的过度产生引发，如家族性 AD 患者和淀粉样前体蛋白转基因动物。
