MRI of hippocampal volume loss in early Alzheimer's disease in relation to ApoE genotype and biomarkers.
MRI of hippocampal volume loss in early Alzheimer's disease in relation to ApoE genotype and biomarkers.
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DOI：
10.1093/brain/awp007
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发表时间：
2009-04
期刊：
影响因子：
--
通讯作者：
Alzheimer's Disease Neuroimaging Initiative
中科院分区：
文献类型：
--
作者：
Schuff N;Woerner N;Boreta L;Kornfield T;Shaw LM;Trojanowski JQ;Thompson PM;Jack CR Jr;Weiner MW;Alzheimer's Disease Neuroimaging Initiative
用MRI测量的海马体积随时间的变化，作为阿尔茨海默病的标志物具有巨大的潜力。本研究的目的是：（i）在阿尔茨海默病神经成像倡议（ADNI）的大型多中心环境中，用MRI测试是否可以在阿尔茨海默病、轻度认知障碍和短时期（例如6-12个月）的正常老化中检测到恒定和加速的海马损失;（ii）确定载脂蛋白E（ApoE）基因多态性调节海马变化的程度;以及（iii）确定海马丢失率是否与阿尔茨海默病的脑脊液（CSF）生物标志物（如β-淀粉样蛋白（Aβ1-42）和tau蛋白（tau））相关。MRI多中心研究包括112名认知正常的老年人，226名轻度认知障碍和96名阿尔茨海默病患者，他们都至少进行了三次连续的MRI扫描，涉及47个不同的成像中心。轻度认知障碍和阿尔茨海默病组显示海马体积在6个月内减少，并在1年内加速减少。此外，海马丢失率的增加与阿尔茨海默病中ApoE等位基因α 4基因的存在以及轻度认知障碍中CSF Aβ1-42的降低相关，与ApoE基因型无关，而与tau蛋白的关系仅为趋势。通过利用连续MRI观察结果之间的统计学相关性，提高了测量海马变化的能力。轻度认知障碍和阿尔茨海默病患者在6个月内海马大量丢失和12个月内海马加速丢失的证明说明了MRI在大型多部位环境中随时间跟踪脑形态变化的能力。此外，在存在ApoE等位基因f14的情况下海马丢失加快与CSF Aβ1-42降低之间的关系支持了海马丢失增加是阿尔茨海默病病理学指标和阿尔茨海默病治疗干预有效性的潜在标志物的概念。
Hippocampal volume change over time, measured with MRI, has huge potential as a marker for Alzheimer's disease. The objectives of this study were: (i) to test if constant and accelerated hippocampal loss can be detected in Alzheimer's disease, mild cognitive impairment and normal ageing over short periods, e.g. 6–12 months, with MRI in the large multicentre setting of the Alzheimer's Disease Neuroimaging Initiative (ADNI); (ii) to determine the extent to which the polymorphism of the apolipoprotein E (ApoE) gene modulates hippocampal change; and (iii) to determine if rates of hippocampal loss correlate with cerebrospinal fluid (CSF) biomarkers of Alzheimer's disease, such as the β-amyloid (Aβ1–42) and tau proteins (tau). The MRI multicentre study included 112 cognitive normal elderly individuals, 226 mild cognitive impairment and 96 Alzheimer's disease patients who all had at least three successive MRI scans, involving 47 different imaging centres. The mild cognitive impairment and Alzheimer's disease groups showed hippocampal volume loss over 6 months and accelerated loss over 1 year. Moreover, increased rates of hippocampal loss were associated with presence of the ApoE allele ɛ4 gene in Alzheimer's disease and lower CSF Aβ1–42 in mild cognitive impairment, irrespective of ApoE genotype, whereas relations with tau were only trends. The power to measure hippocampal change was improved by exploiting correlations statistically between successive MRI observations. The demonstration of considerable hippocampal loss in mild cognitive impairment and Alzheimer's disease patients over only 6 months and accelerated loss over 12 months illustrates the power of MRI to track morphological brain changes over time in a large multisite setting. Furthermore, the relations between faster hippocampal loss in the presence of ApoE allele ɛ4 and decreased CSF Aβ1–42 supports the concept that increased hippocampal loss is an indicator of Alzheimer's disease pathology and a potential marker for the efficacy of therapeutic interventions in Alzheimer's disease.
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