Neurology-主动脉僵化或提示神经炎症和神经变性

2021-06-17 Freeman MedSci原创

主动脉僵化或提示神经炎症和神经变性

与年龄有关的动脉僵化(arterial stiffening),通常用脉搏波速度(pulse wave velocity)评估,与认知障碍、大脑结构变化和脑小血管疾病有关。

由于弹性动脉,如主动脉,随着年龄的增长而变硬,它们不太能够缓冲血液脉动的正常变化。脉动的增加损害了脑部微循环,导致血流的减少。然而,微循环变化所导致的或加剧的分子病理学仍然是未知的。

以前的研究已经调查了血管僵化和阿尔茨海默病(AD)核心病理之间的联系,即淀粉样蛋白-β(Ab)和磷酸化tau(p-tau)。使用不太敏感的动脉僵化措施,僵化的增加与更大的脑部Ab和p-tau沉积有关。大脑缺氧会导致轴突病变和总tau(t-tau,AD型神经变性的标志)增加,这表明亚临床动脉僵化可能影响大脑健康的其他途径。

此外,鉴于毛细血管损伤后小胶质细胞和星形细胞的激活,血液脉动的增加可能会导致神经炎症的级联反应。然而,与年龄相关的主动脉僵硬度的细微增加与伴随的损伤途径有什么关系仍未知。

藉此,Vanderbilt University Medical Center的 Elizabeth E Moore等人,探究了无临床痴呆的老年人中央主动脉僵硬度和脑脊液(CSF)生物标志物证据(Ab,p-tau)、AD型神经变性(t-tau)、突触功能障碍(神经粒蛋白)、神经轴损伤(神经丝光(NFL))和神经炎症(YKL-40,可溶性触发受体在骨髓细胞上表达2(sTREM2))之间的关系。


他们利用范德比尔特记忆和老龄化项目,其参与者没有中风和痴呆,这是一项基于社区的观察性研究,他们接受了心脏磁共振评估主动脉脉搏波速度(PWV,米/秒)和腰椎穿刺以获得CSF。通过线性回归将主动脉脉搏波速度与CSF Aβ、p-tau、t-tau、神经粒蛋白、NFL、YKL-40和sTREM2的浓度联系起来,调整了年龄、种族/民族、教育、脂蛋白(APOE)ε4状态、弗雷明汉中风风险档案和认知诊断

146名参与者接受了检查(72±6岁)。他们发现,主动脉脉搏波速度与年龄在p-tau(β=0.31,p=0.04)、t-tau(β=2.67,p=0.05)、neurogranin(β=0.94,p=0.04)和sTREM2(β=20.4,p=0.05)上相互作用。

在73岁以上的参与者中,较高的主动脉脉搏波速度与较高的p-tau(β=2.4,p=0.03)、t-tau(β=19.3,p=0.05)、Neurogranin(β=8.4,p=0.01)和YKL-40浓度(β=7880,p=0.005)有关。

主动脉脉搏波速度与诊断对神经粒蛋白的影响(β=-10.76,p=0.03)和高血压状态对YKL-40的影响(β=-18020,p<0.001)有适度的相互作用。

这个研究的主要意义在于,发现了再最年长的参与者中( >74岁),更大的主动脉僵化与神经炎症、tau磷酸化、突触功能障碍和神经变性的体内生物标志物证据有关,但不是淀粉样变。中央动脉僵化可能导致累积的脑微循环损伤和组织的血流输送,导致更高年龄的神经炎症和神经变性。

原文出处:
Association of Aortic Stiffness With Biomarkers of Neuroinflammation, Synaptic Dysfunction, and Neurodegeneration
Elizabeth E Moore, Dandan Liu, et al., Angela L Jefferson
Neurology May 2021, 10.1212/WNL.0000000000012257; DOI: 10.1212/WNL.0000000000012257

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    2021-10-15 yinhl1978
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    2021-06-18 huangdf
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    2021-06-17 亭儿789

    倒是一个新话题

    0

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