From the Department of Radiology & Nuclear Medicine (R.O., S.C.J.V., H.V., A.V., R.A.v.S., S.M.A., M.D.Z., R.B., A.D.W., F.B., A.A.L., B.N.M.v.B.), Alzheimer Center & Department of Neurology, Neuroscience Campus Amsterdam (R.O., W.M.v.d.F., S.A.S., S.M.A., M.D.Z., P.S.), and Department of Epidemiology & Biostatistics (W.M.v.d.F., S.A.S., J.T.), VU University Medical Center, Amsterdam, the Netherlands.
Neurology. 2014 May 20;82(20):1768-75. doi: 10.1212/WNL.0000000000000432. Epub 2014 Apr 18.
To assess how amyloid deposition, glucose hypometabolism, and cerebral atrophy affect neuropsychological performance in patients with Alzheimer disease (AD) dementia, patients with mild cognitive impairment (MCI), and controls over time.
A total of 41 patients with AD dementia, 28 patients with MCI, and 19 controls underwent [(11)C]-Pittsburgh compound B ((11)C-PiB) and [(18)F]-2-fluoro-2-deoxy-d-glucose ((18)F-FDG)-PET and MRI scans at baseline. We extracted global binding potential for (11)C-PiB, the number of abnormal voxels for (18)F-FDG, and gray matter volumes using SIENAX for MRI as measures of amyloid, hypometabolism, and atrophy. In addition, repeat neuropsychological testing was performed, including memory, attention, language, and executive tasks (mean follow-up 2.2 ± 0.7 years). Cross-sectional and longitudinal relationships between imaging markers and cognition were assessed using linear mixed models, including terms for the imaging markers, time, sex, age, diagnosis, and interactions for imaging marker × time and imaging marker × time × diagnosis.
Linear mixed models showed that baseline hypometabolism and atrophy were associated with poorer baseline performance on attention and executive functions (p < 0.05), whereas amyloid was not related to baseline cognition. Hypometabolism and amyloid were strongly associated with longitudinal decline in essentially all cognitive domains (pinteraction < 0.05), whereas atrophy was related specifically to future decline in Mini-Mental State Examination and memory (pinteraction < 0.05).
Glucose hypometabolism and brain atrophy were associated with concurrent cognitive function, whereas brain amyloid was not. Amyloid deposition and glucose hypometabolism were predictors for decline of a wide variety of cognitive functions, while brain atrophy specifically predicted memory deterioration.
评估淀粉样蛋白沉积、葡萄糖代谢低下和脑萎缩如何影响阿尔茨海默病（AD）痴呆患者、轻度认知障碍（MCI）患者和对照组患者的神经心理学表现。
共纳入 41 例 AD 痴呆患者、28 例 MCI 患者和 19 例对照组患者，在基线时进行 [(11)C]-匹兹堡化合物 B（(11)C-PiB）和 [(18)F]-2-氟-2-脱氧-D-葡萄糖（(18)F-FDG）-PET 和 MRI 扫描。我们使用 SIENAX 提取 [(11)C-PiB 的全局结合势、(18)F-FDG 的异常体素数量和灰质体积，作为淀粉样蛋白、代谢低下和萎缩的测量指标。此外，进行了重复的神经心理学测试，包括记忆、注意力、语言和执行任务（平均随访时间为 2.2±0.7 年）。使用线性混合模型评估影像学标志物和认知之间的横断面和纵向关系，包括影像学标志物、时间、性别、年龄、诊断以及影像学标志物×时间和影像学标志物×时间×诊断的交互项。
线性混合模型显示，基线时代谢低下和萎缩与注意力和执行功能的基线表现较差相关（p<0.05），而淀粉样蛋白与基线认知无关。代谢低下和淀粉样蛋白与几乎所有认知领域的纵向下降密切相关（p 交互<0.05），而萎缩仅与未来的简易精神状态检查和记忆下降相关（p 交互<0.05）。
葡萄糖代谢低下和脑萎缩与认知功能有关，而脑淀粉样蛋白则无。淀粉样蛋白沉积和葡萄糖代谢低下是多种认知功能下降的预测因素，而脑萎缩则特异性地预测记忆恶化。
