Distribution of Amyloid Burden Differs between Idiopathic Normal Pressure Hydrocephalus and Alzheimer's Disease
Distribution of Amyloid Burden Differs between Idiopathic Normal Pressure Hydrocephalus and Alzheimer's Disease
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DOI：
10.1177/197140091302600107
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发表时间：
2013-02-01
影响因子：
1.2
通讯作者：
Nakagawa, M.
中科院分区：
文献类型：
--
作者：
Kondo, M.;Tokuda, T.;Nakagawa, M.
本研究旨在阐明匹兹堡化合物B （PIB）皮层滞留在特发性常压脑积水（iNPH）患者中的发生率和分布，并澄清其与阿尔茨海默病（AD）患者的差异。本研究纳入了10例无任何AD临床体征的iNPH患者。比较了7例年龄匹配的AD患者在iNPH患者正电子发射断层扫描（PET）中PIB的脑保留情况。脑脊液β -淀粉样蛋白1-42肽（A β 42）水平也被测量，其与脑淀粉样蛋白负荷呈负相关下降。10例iNPH患者中有3例显示皮质PIB潴留增加。尽管平均皮质SUV比率相似，但iNPH和AD患者的PIB保留分布差异很大。在iNPH患者中，PIB保留仅限于高凸起的旁矢状区，而在AD患者中，PIB保留则扩散到额叶和顶叶区。在评价皮质PIB保留的分布模式方面，PIB- pet的冠状面图像比传统的横向图像更有价值。两名皮质PIB潴留较高的iNPH患者脑脊液A β 42水平最低，表明iNPH中PIB潴留并不反映PIB清除的简单延迟，而是与大脑中存在的A β淀粉样蛋白结合。我们的结果表明，iNPH是表现皮层PIB保留的疾病之一。PIB保留在iNPH中的特征性分布可用于iNPH与AD的鉴别诊断。
This study aimed to elucidate the incidence and distribution of the cortical retention of Pittsburgh compound B (PIB) in patients with idiopathic normal pressure hydrocephalus (iNPH) and clarify the differences from those in patients with Alzheimer's disease (AD). Ten patients with iNPH without any clinical signs indicative of AD were enrolled in this study. Cerebral retention of PIB in positron emission tomography (PET) in iNPH patients was compared with those in seven age-matched AD patients. The CSF levels of beta-amyloid 1-42 peptide (A beta 42), which inversely decrease with cerebral amyloid burden, were also measured. Three of the ten patients with iNPH showed increased cortical PIB retention. Although the mean cortical SUV ratios were similar, the distribution of PIB retention differed widely between the patients with iNPH and AD. PIB retention was limited to the high-convexity parasagittal areas in iNPH patients, whereas it spread over the frontal and parietotemporal areas in AD. The coronal images of PIB-PET were more informative than conventional transverse images in evaluating the distribution pattern of cortical PIB retention. Two iNPH patients with higher cortical PIB retention had the lowest levels of CSF A beta 42, indicating that PIB retention in iNPH would not reflect a simple delay in PIB clearance but its binding to existing A beta amyloid in the brain. Our results indicate that iNPH is one of the diseases exhibiting cortical PIB retention. The characteristic distribution of PIB retention in iNPH could be useful in the differential diagnosis between iNPH and AD.