Department of Psychiatry, National Center for Geriatrics and Gerontology, Japan.
Department of Neurology, National Cerebral and Cardiovascular Center, Suita, Japan.
Int J Geriatr Psychiatry. 2019 Nov;34(11):1651-1657. doi: 10.1002/gps.5178. Epub 2019 Jul 31.
A direct causal relationship of cerebrovascular risk factors/stroke to amyloid β (Aβ) deposition has yet to be shown. We conducted [ C] Pittsburgh compound B (PiB)-positron emission tomography (PET) analysis on subacute ischemic stroke patients and healthy controls. We hypothesized that subacute ischemic stroke patients would show focal Aβ accumulation in cortical regions, which would increase and extend over time during the chronic phase after stroke onset.
Patients were recruited 14 to 28 days after acute subcortical ischemic stroke and examined with [ C]PiB-PET scans. Regional time-activity data were analyzed with the Logan graphical method. Whole brain voxel-based analysis was conducted to compare stroke patients with healthy controls. We also performed longitudinal comparison of patients with successive [ C]PiB-PET scans 1 year after stroke.
Voxel-based analysis revealed a significant increase of [ C]PiB-BP of the precuneus/posterior cingulate cortex (PCu/PCC) in stroke patients at the subacute stage. Based on stepwise multiple regression analysis of [ C]PiB-BP changes during follow-up as the dependent variable, years of education was the best independent correlate. There was a significant negative relationship between changes in [ C]PiB-BP and years of education.
Our results suggest that processes before and after the onset of ischemic stroke may trigger Aβ deposition in the PCu/PCC, whereby amyloid deposition begins at an early stage of Alzheimer's disease (AD). Our findings support the existence of a cooperative association between vascular risk factors/stroke and AD progression. Further, educational achievement had a protective effect against the increase in Aβ accumulation.
尚未证明脑血管危险因素/中风与淀粉样蛋白β（Aβ）沉积之间存在直接因果关系。我们对亚急性缺血性中风患者和健康对照者进行了[C]匹兹堡化合物 B（PiB）-正电子发射断层扫描（PET）分析。我们假设亚急性缺血性中风患者会在皮质区域出现局灶性 Aβ积聚，这种积聚会在中风发作后的慢性期内逐渐增加和扩大。
患者在急性皮质下缺血性中风后 14 至 28 天内被招募，并接受[C]PiB-PET 扫描。使用 Logan 图形法分析区域时间活动数据。采用基于体素的方法比较中风患者和健康对照组。我们还对中风后 1 年进行连续[C]PiB-PET 扫描的患者进行了纵向比较。
基于体素的分析显示，在亚急性期中风患者中，楔前叶/后扣带回皮质（PCu/PCC）的[C]PiB-BP 显著增加。基于对随访期间[C]PiB-BP 变化作为因变量的逐步多元回归分析，受教育年限是最佳的独立相关因素。[C]PiB-BP 变化与受教育年限之间存在显著的负相关关系。
我们的研究结果表明，中风发作前后的过程可能会引发 PCu/PCC 中的 Aβ沉积，从而表明淀粉样蛋白沉积始于阿尔茨海默病（AD）的早期阶段。我们的发现支持血管危险因素/中风与 AD 进展之间存在协同关联的存在。此外，教育程度对 Aβ积聚增加具有保护作用。
