Comparison of cerebrospinal fluid profiles in Alzheimer’s disease with multiple cerebral microbleeds and cerebral-amyloid angiopathy related inflammation.
Comparison of cerebrospinal fluid profiles in Alzheimer’s disease with multiple cerebral microbleeds and cerebral-amyloid angiopathy related inflammation.
复制标题
阿尔茨海默病与多发性脑微出血和脑淀粉样血管病相关炎症的脑脊液特征的比较。
DOI：
10.1007/s00415-016-8362-2
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发表时间：
2017
影响因子：
6
通讯作者：
Inuzuka T.
中科院分区：
文献类型：
--
作者：
Kimura A;Takemura M;Kuniaki S;Yoshikura N;Hayashi Y;Harada N;Nishida H;Nakajima H;Inuzuka T.
阿尔茨海默病（AD）患者的脑磁共振成像（MRI）有时显示多发性脑微出血（CMB）和融合性白色高信号（WMH），与脑淀粉样血管病相关炎症（CAA-I）相似。为了确定是否有可能是共同的病理生理机制的MRI结果的多个CMB和融合的WMH，我们调查了脑脊液（CSF）的38 AD，5遗忘型轻度认知功能障碍（MCI），和6 CAA-I患者的配置文件。AD和MCI患者分为脑MRI T2* 梯度回波序列有或无多发性CMB组（n= 33）。我们比较了AD和MCI伴或不伴多发性CMB患者以及CAA-I患者的CSF特征。多发性CMB患者的脑MRI显示与无多发性CMB患者相比，严重程度的WMH。CAA-I组脑脊液抗淀粉样蛋白β自身抗体、白细胞介素8水平、脑脊液/血清白蛋白比值及免疫球蛋白G指数均显著高于其他组。然而，有或没有多个CMB的患者的CSF特征没有显著差异。我们的研究为AD和CAA-I中这些差异性MRI结果的不同病理生理机制提供了证据。
Brain magnetic resonance imaging (MRI) of patients with Alzheimer’s disease (AD) sometimes reveals multiple cerebral microbleeds (CMBs) and confluent white matter hyperintensities (WMHs) similar to those observed in cerebral amyloid angiopathy-related inflammation (CAA-I). To determine whether there might be common pathophysiological mechanisms underlying the MRI findings of multiple CMBs and confluent WMHs, we investigated the cerebrospinal fluid (CSF) profiles of 38 AD, five amnestic mild cognitive impairment (MCI), and six CAA-I patients. The AD and MCI patients were divided into groups of patients with (n= 10) or without (n= 33) multiple CMBs (n≥ 2) on T2*-gradient echo sequences of brain MRI. We compared the CSF profiles of AD and MCI patients with or without multiple CMBs, and CAA-I patients. The brain MRIs of the patients with multiple CMBs revealed severe degrees of WMHs compared with the patients without multiple CMBs. The levels of CSF anti-amyloid β autoantibody and interleukin 8, and CSF/serum albumin ratios and immunoglobulin G indexes, were significantly higher in CAA-I patients than the other groups. However, there were no significant differences in the CSF profiles of patients with or without multiple CMBs. Our study provides evidence for different pathophysiological mechanisms underlying these differential MRI findings in AD and CAA-I.