Centre of Excellence for Alzheimer's Disease Research and Care, School of Medical Sciences, Edith Cowan University, Joondalup, WA, Australia.
Mol Psychiatry. 2013 Aug;18(8):875-81. doi: 10.1038/mp.2012.107. Epub 2012 Aug 14.
Previous studies suggest physical activity improves cognition and lowers Alzheimer's disease (AD) risk. However, key AD pathogenic factors that are thought to be influenced by physical activity, particularly plasma amyloid-β (Aβ) and Aβ brain load, have yet to be thoroughly investigated. The objective of this study was to determine if plasma Aβ and amyloid brain deposition are associated with physical activity levels, and whether these associations differed between carriers and non-carriers of the apolipoprotein E (APOE) ε4 allele. Five-hundred and forty six cognitively intact participants (aged 60-95 years) from the Australian Imaging, Biomarkers and Lifestyle Study of Ageing (AIBL) were included in these analyses. Habitual physical activity levels were measured using the International Physical Activity Questionnaire (IPAQ). Serum insulin, glucose, cholesterol and plasma Aβ levels were measured in fasting blood samples. A subgroup (n=116) underwent (11)C-Pittsburgh compound B (PiB) positron emission tomography (PET) scanning to quantify brain amyloid load. Higher levels of physical activity were associated with higher high density lipoprotein (HDL) (P=0.037), and lower insulin (P<0.001), triglycerides (P=0.019) and Aβ1-42/1-40 ratio (P=0.001). After stratification of the cohort based on APOE ε4 allele carriage, it was evident that only non-carriers received the benefit of reduced plasma Aβ from physical activity. Conversely, lower levels of PiB SUVR (standardised uptake value ratio) were observed in higher exercising APOE ε4 carriers. Lower plasma Aβ1-42/1-40 and brain amyloid was observed in those reporting higher levels of physical activity, consistent with the hypothesis that physical activity may be involved in the modulation of pathogenic changes associated with AD.
先前的研究表明，身体活动可以改善认知能力并降低阿尔茨海默病（AD）的风险。然而，身体活动被认为可以影响关键的 AD 致病因素，特别是血浆淀粉样蛋白-β（Aβ）和 Aβ脑负荷，但这些因素尚未得到彻底研究。本研究的目的是确定血浆 Aβ和淀粉样蛋白脑沉积是否与身体活动水平相关，以及这些关联在载脂蛋白 E（APOE）ε4 等位基因携带者和非携带者之间是否存在差异。本研究分析了来自澳大利亚成像、生物标志物和生活方式研究衰老（AIBL）的 546 名认知正常的参与者（年龄 60-95 岁）。使用国际体力活动问卷（IPAQ）测量习惯性身体活动水平。在空腹血样中测量血清胰岛素、葡萄糖、胆固醇和血浆 Aβ水平。亚组（n=116）接受了（11）C-匹兹堡化合物 B（PiB）正电子发射断层扫描（PET）扫描，以定量大脑淀粉样蛋白负荷。更高水平的身体活动与更高的高密度脂蛋白（HDL）（P=0.037）、更低的胰岛素（P<0.001）、甘油三酯（P=0.019）和 Aβ1-42/1-40 比值（P=0.001）相关。根据 APOE ε4 等位基因携带情况对队列进行分层后，很明显只有非携带者从身体活动中受益于降低血浆 Aβ。相反，在高水平运动的 APOE ε4 携带者中，PiB SUVR（标准化摄取值比）水平较低。在报告高水平身体活动的人群中观察到较低的血浆 Aβ1-42/1-40 和脑淀粉样蛋白，这与身体活动可能参与调节与 AD 相关的致病变化的假说一致。
