Department of Radiology, Mayo Clinic and Foundation, 200 First St SW, Rochester, MN 55905, USA.
Ann Neurol. 2012 Nov;72(5):730-8. doi: 10.1002/ana.23665.
A study was undertaken to investigate the association of intellectual and physical activity with biomarkers of Alzheimer disease (AD) pathophysiology and cognition in a nondemented elderly population. The biomarkers evaluated were brain Aβ load via Pittsburgh compound B (PiB)-positron emission tomography (PET), neuronal dysfunction via (18) F-fluorodeoxyglucose (FDG)-PET, and neurodegeneration via structural magnetic resonance imaging (MRI).
We studied 515 nondemented (428 cognitively normal and 87 mild cognitive impairment) participants in the population-based Mayo Clinic Study of Aging who completed a 3T MRI, PET scans, and APOE genotype, and had lifestyle activity measures and cognition data available. The imaging measures computed were global PiB-PET uptake, and global FDG-PET and MRI based hippocampal volume. We consolidated activity variables into lifetime intellectual, current intellectual, and current physical activities. We used a global cognitive z score as a measure of cognition. We applied 2 independent methods-partial correlation analysis adjusted for age and gender and path analysis using structural equations-to evaluate the associations between lifestyle activities, imaging biomarkers, and global cognition.
None of the lifestyle variables were correlated with the biomarkers, and the path associations between lifestyle variables and biomarkers were not significant (p > 0.05). Conversely, all the biomarkers were correlated with global cognitive z score (p < 0.05), and the path associations between (lifetime and current) intellectual activities and global z score were significant (p < 0.01).
Intellectual and physical activity lifestyle factors were not associated with AD biomarkers, but intellectual lifestyle factors explained variability in the cognitive performance in this nondemented population. This study provides evidence that lifestyle activities may delay the onset of dementia but do not significantly influence the expression of AD pathophysiology.
本研究旨在调查智力和身体活动与阿尔茨海默病（AD）病理生理学和认知的生物标志物在非痴呆老年人群中的关联。评估的生物标志物包括通过匹兹堡化合物 B（PiB）正电子发射断层扫描（PET）评估脑 Aβ 负荷、通过（18）F-氟脱氧葡萄糖（FDG）-PET 评估神经元功能障碍、以及通过结构磁共振成像（MRI）评估神经退行性变。
我们研究了 515 名非痴呆（428 名认知正常和 87 名轻度认知障碍）参与者，这些参与者来自基于人群的 Mayo 诊所衰老研究，他们完成了 3T MRI、PET 扫描和 APOE 基因型，并可获得生活方式活动测量和认知数据。计算的影像学测量值包括全局 PiB-PET 摄取、全局 FDG-PET 和基于 MRI 的海马体积。我们将活动变量整合为终生智力、当前智力和当前体力活动。我们使用整体认知 z 分数作为认知的衡量标准。我们应用了 2 种独立的方法——偏相关分析，调整年龄和性别因素，以及使用结构方程的路径分析——来评估生活方式活动、影像学生物标志物和整体认知之间的关联。
没有一个生活方式变量与生物标志物相关，生活方式变量与生物标志物之间的路径关联没有统计学意义（p>0.05）。相反，所有的生物标志物都与整体认知 z 分数相关（p<0.05），而（终生和当前）智力活动与整体 z 分数之间的路径关联具有统计学意义（p<0.01）。
智力和身体活动生活方式因素与 AD 生物标志物无关，但智力生活方式因素可以解释该非痴呆人群认知表现的变异性。本研究提供了证据表明，生活方式活动可能会延迟痴呆的发病，但对 AD 病理生理学的表达没有显著影响。
