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有氧运动可改善高血压载脂蛋白 E4 携带者的海马血流。

Aerobic exercise improves hippocampal blood flow for hypertensive Apolipoprotein E4 carriers.

机构信息

Department of Molecular & Integrative Physiology, University of Kansas Medical Center, Kansas City, KS, USA.

University of Kansas Alzheimer's Disease Center, Fairway, KS, USA.

出版信息

J Cereb Blood Flow Metab. 2021 Aug;41(8):2026-2037. doi: 10.1177/0271678X21990342. Epub 2021 Jan 28.

Abstract

Cerebrovascular dysfunction likely contributes causally to Alzheimer's disease (AD). The strongest genetic risk factor for late-onset AD, (), may act synergistically with vascular risk to cause dementia. Therefore, interventions that improve vascular health, such as exercise, may be particularly beneficial for carriers. We assigned cognitively normal adults (65-87 years) to an aerobic exercise intervention or education only. Arterial spin labeling MRI measured hippocampal blood flow (HBF) before and after the 52-week intervention. We selected participants with hypertension at enrollment (n = 44). For carriers, change in HBF (ΔHBF) was significantly ( = 0.006) higher for participants in the exercise intervention (4.09 mL/100g/min) than the control group (-2.08 mL/100g/min). There was no difference in ΔHBF between the control (-0.32 mL/100g/min) and exercise (-0.54 mL/100g/min) groups for non-carriers (p = 0.918). Additionally, a multiple regression showed an interaction between change in systolic blood pressure (ΔSBP) and carrier status on ΔHBF ( = 0.035), with reductions in SBP increasing HBF for carriers only. Aerobic exercise improved HBF for hypertensive carriers only. Additionally, only carriers exhibited an inverse relationship between ΔSBP and ΔHBF. This suggests exercise interventions, particularly those that lower SBP, may be beneficial for individuals at highest genetic risk of AD.: .

摘要

脑血管功能障碍可能是导致阿尔茨海默病(AD)的原因。最强的晚发性 AD 遗传风险因素 APOE ε4,可能与血管风险协同作用导致痴呆。因此,改善血管健康的干预措施,如运动,可能对携带者特别有益。我们将认知正常的成年人(65-87 岁)分配到有氧运动干预组或仅接受教育组。动脉自旋标记 MRI 在 52 周干预前后测量海马血流(HBF)。我们在入组时选择了患有高血压的参与者(n=44)。对于携带者,运动干预组的 HBF 变化(ΔHBF)明显更高( = 0.006),为 4.09 mL/100g/min,而对照组为-2.08 mL/100g/min。非携带者的对照组(-0.32 mL/100g/min)和运动组(-0.54 mL/100g/min)之间的 ΔHBF 没有差异(p = 0.918)。此外,多元回归显示,收缩压变化(ΔSBP)与携带者状态对 ΔHBF 的交互作用( = 0.035),SBP 降低仅增加携带者的 HBF。有氧运动仅改善高血压携带者的 HBF。此外,只有携带者表现出 ΔSBP 和 ΔHBF 之间的反比关系。这表明运动干预,特别是那些降低 SBP 的干预措施,可能对 AD 遗传风险最高的个体有益。

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