Translational Neuroimaging Laboratory, The McGill University Research Centre for Studies in Aging, Montreal, Canada.
Translational Neuroimaging Laboratory, The McGill University Research Centre for Studies in Aging, Montreal, Canada; CAPES Foundation, Ministry of Education of Brazil, Brasília, Brazil.
Alzheimers Dement. 2017 Jun;13(6):644-653. doi: 10.1016/j.jalz.2016.11.005. Epub 2016 Dec 23.
Recent literature proposes that amyloid β (Aβ) and phosphorylated tau (p-tau) synergism accelerates biomarker abnormalities in controls. Yet, it remains to be answered whether this synergism is the driving force behind Alzheimer disease (AD) dementia.
We stratified 314 mild cognitive impairment individuals using [F]florbetapir positron emission tomography Aβ imaging and cerebrospinal fluid p-tau. Regression and voxel-based logistic regression models with interaction terms evaluated 2-year changes in cognition and clinical status as a function of baseline biomarkers.
We found that the synergism between [F]florbetapir and p-tau, rather than their additive effects, was associated with the cognitive decline and progression to AD. Furthermore, voxel-based analysis revealed that temporal and inferior parietal were the regions where the synergism determined an increased likelihood of developing AD.
Together, the present results support that progression to AD dementia is driven by the synergistic rather than a mere additive effect between Aβ and p-tau proteins.
最近的文献表明，β淀粉样蛋白（Aβ）和磷酸化 tau（p-tau）的协同作用加速了对照者的生物标志物异常。然而，Aβ 和 p-tau 的这种协同作用是否是阿尔茨海默病（AD）痴呆的驱动因素仍有待回答。
我们使用 [F]florbetapir 正电子发射断层扫描 Aβ 成像和脑脊液 p-tau 对 314 名轻度认知障碍个体进行分层。回归和基于体素的逻辑回归模型与交互项评估了认知和临床状态在 2 年内的变化，作为基线生物标志物的函数。
我们发现，[F]florbetapir 和 p-tau 之间的协同作用，而不是它们的加性效应，与认知下降和进展为 AD 有关。此外，基于体素的分析显示，颞叶和顶下小叶是协同作用导致 AD 发生可能性增加的区域。
总之，目前的结果支持 AD 痴呆的进展是由 Aβ 和 p-tau 蛋白之间的协同作用而不是单纯的加性效应驱动的。
