ImFINE Research Group, Department of Health and Human Performance, Universidad Politécnica de Madrid, Spain; EXERNET Spanish Research Network on Physical Exercise and Health, Spain.
Helen Wills Neuroscience Institute, University of California Berkeley, USA.
J Sci Med Sport. 2024 Jun;27(6):402-407. doi: 10.1016/j.jsams.2024.03.012. Epub 2024 Apr 3.
To investigate if higher baseline physical activity levels are associated with less β-amyloid burden and whether the ApoE4 genotype moderates this association cross-sectionally and longitudinally.
Prospective cohort study.
204 cognitively normal older adults (74.5 ± 6.6 years; 26 % ApoE4-carrier) were analyzed. Baseline physical activity was measured using the Minnesota Physical Activity Questionnaire. Brain β-amyloid burden was measured with positron emission tomography using 11C-labeled Pittsburgh compound. A subsample of 128 participants underwent longitudinal positron emission tomography (2.0 ± 0.9 scans over 5 ± 3 years). Statistical analysis was run according to physical activity (high/low group) and the ApoE4 genotype (carrier/noncarrier).
The ApoE4 genotype moderated the relationship between physical activity and β-amyloid, such that low physical activity had a greater impact on β-amyloid deposition in ApoE4-carriers than noncarriers. This ApoE4 × physical activity effect on brain β-amyloid deposition was also observed when all available β-amyloid scan timepoints were included in the model. β-amyloid deposition increased over time (p < 0.001), and ApoE4-carriers had disproportionately greater β-amyloid accumulation than ApoE4-noncarriers. The lower physical activity group had marginally greater β-amyloid accumulation than the higher physical activity group (p = 0.099), but there was no significant ApoE4 effect on β-amyloid accumulation.
Low physical activity in combination with the ApoE4-carrier genotype is associated with increased β-amyloid burden, suggesting that ApoE4 moderates the effect of physical activity on β-amyloid load. However, this effect was insufficient for baseline physical activity to modulate the change in β-amyloid accumulation over time.
探究基线时较高的身体活动水平是否与β-淀粉样蛋白负担较低相关，以及载脂蛋白 E4（ApoE4）基因型是否会横向和纵向调节这种关联。
前瞻性队列研究。
对 204 名认知正常的老年人（74.5±6.6 岁；26%为 ApoE4 携带者）进行了分析。基线身体活动通过明尼苏达州身体活动问卷进行测量。使用 11C 标记的匹兹堡化合物通过正电子发射断层扫描（PET）测量脑内β-淀粉样蛋白负担。128 名参与者的亚组接受了纵向 PET（5±3 年内进行 2.0±0.9 次扫描）。根据身体活动（高/低组）和 ApoE4 基因型（携带者/非携带者）进行统计分析。
ApoE4 基因型调节了身体活动与β-淀粉样蛋白之间的关系，使得低身体活动对 ApoE4 携带者的β-淀粉样蛋白沉积的影响大于非携带者。当将所有可用的β-淀粉样蛋白扫描时间点纳入模型时，也观察到 ApoE4×身体活动对脑β-淀粉样蛋白沉积的影响。β-淀粉样蛋白沉积随时间增加（p<0.001），ApoE4 携带者的β-淀粉样蛋白积累不成比例地高于 ApoE4 非携带者。低身体活动组的β-淀粉样蛋白积累比高身体活动组稍高（p=0.099），但 ApoE4 对β-淀粉样蛋白积累没有显著影响。
低身体活动与 ApoE4 携带者基因型相结合与β-淀粉样蛋白负担增加相关，表明 ApoE4 调节身体活动对β-淀粉样蛋白负荷的影响。然而，这种影响不足以使基线身体活动调节随时间推移β-淀粉样蛋白积累的变化。
