摘要
阿尔茨海默氏病(AD)是最常见的神经退行性疾病,病理特征是β淀粉样蛋白(Aβ)斑块和神经原纤维缠结。AD发生tau蛋白病理改变前已经产生β淀粉样蛋白聚集,然而,由一个的聚集形式有助于皮质变薄的机制和两者之间的因果关系的病理和机制还没有完全理解。我们在AD患者的图像提出了通过磁共振(MR)和匹兹堡化合物B(PIB)正电子发断层扫描(PET)定量β淀粉样蛋白加权皮层厚度以分析探讨皮质变薄和淀粉样斑块沉积区域之间的关系,有利于轻度认知障碍(MCI)认知主体。本研究利用磁共振成像和PIB、PET数据来了解阿尔茨海默病的神经影像学表现。我们测量比较AD,MCI三双不同的分类模型的精度,与认知正常。使用β-加权皮质厚度的分类模型并不逊色于只使用皮质厚度或淀粉样沉积的分类模型。此外,基于时间的变化在皮质变薄和β淀粉样蛋白沉积如β淀粉样蛋白沉积后皮质变薄;皮质变薄后β沉积,或并发β沉积和皮质变薄,我们确定了皮质变薄与β淀粉样蛋白沉积之间的三种关系类型。(1)β淀粉样蛋白相关型皮质变薄;(2)独立于β淀粉样蛋白型皮质变薄;(3)单纯型β淀粉样蛋白沉积无皮质变薄。总之,这些研究结果表明,β淀粉样蛋白-加权皮质厚度值可以用来作为脑淀粉样病变所造成的结构变化的一个客观的生物标志物。
关键词: 阿尔茨海默氏病,β淀粉样蛋白,淀粉样蛋白成像,β淀粉样蛋白-加权皮质厚度,磁共振,轻度认知功能障碍,认知正常,tau蛋白
Current Alzheimer Research
Title:Amyloid Beta-Weighted Cortical Thickness: A New Imaging Biomarker in Alzheimer's Disease
Volume: 12 Issue: 6
Author(s): Chan Mi Kim, Jihye Hwang, Jong-Min Lee, Jee Hoon Roh, Jae-Hong Lee, Jae-Young Koh and Alzheimer’s Disease Neuroimaging Initiativ
Affiliation:
关键词: 阿尔茨海默氏病,β淀粉样蛋白,淀粉样蛋白成像,β淀粉样蛋白-加权皮质厚度,磁共振,轻度认知功能障碍,认知正常,tau蛋白
摘要: Alzheimer’s disease (AD) is the most common neurodegenerative disorder pathologically characterized by amyloid-beta (Aβ) plaques and neurofibrillary tangles. The aggregation of Aβ precedes tau pathologies in AD; however, the causal relation between the two pathologies and the mechanisms by which aggregated forms of Aβ contribute to cortical thinning are not fully understood. We proposed quantitative Aβ-weighted cortical thickness analysis to investigate the regional relationship between cortical thinning and amyloid plaque deposition using magnetic resonance (MR) and Pittsburg Compound B (PiB) positron emission tomography (PET) images in patients with AD, mild cognitive impairment (MCI), and subjects with normal cognition. We hypothesized that there are cortical areas that have prominent changes associated with Aβ deposition and there are areas that are relatively independent from Aβ deposition where pathologies other than Aβ (such as tau) are predominant. The study was performed using MRI and PiB PET data from the Alzheimer’s Disease Neuroimaging Initiative. We measured accuracy of classification models in three different pairs of groups comparing AD, MCI, and normal cognition. Classification models that used Aβ-weighted cortical thickness were not inferior to classification models that used only cortical thickness or amyloid deposition. In addition, based on timing of changes in cortical thinning and Aβ deposition such as Aβ deposition after cortical thinning; cortical thinning after Aβ deposition, or concurrent Aβ deposition and cortical thinning, we identified three types of relationships between cortical thinning and Aβ deposition: (1) Aβ-associated cortical thinning; (2) Aβ-independent cortical thinning; and (3) Aβ deposition only without cortical thinning. Taken together, these findings suggest that Aβ-weighted cortical thickness values can be used as an objective biomarker of structural changes caused by amyloid pathology in the brain.
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Cite this article as:
Chan Mi Kim, Jihye Hwang, Jong-Min Lee, Jee Hoon Roh, Jae-Hong Lee, Jae-Young Koh and Alzheimer’s Disease Neuroimaging Initiativ , Amyloid Beta-Weighted Cortical Thickness: A New Imaging Biomarker in Alzheimer's Disease, Current Alzheimer Research 2015; 12 (6) . https://dx.doi.org/10.2174/1567205012666150530202124
DOI https://dx.doi.org/10.2174/1567205012666150530202124 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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