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首页> 外文期刊>JAMA neurology >Interactive Associations of Vascular Risk and β-Amyloid Burden With Cognitive Decline in Clinically Normal Elderly IndividualsFindings From the Harvard Aging Brain Study
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Interactive Associations of Vascular Risk and β-Amyloid Burden With Cognitive Decline in Clinically Normal Elderly IndividualsFindings From the Harvard Aging Brain Study

机译：兔近年脑卒中脑卒中脑卒中脑卒中脑卒中临床正常年龄闭塞性患者血管风险和β-淀粉样沉重的互动联想

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Importance? Identifying asymptomatic individuals at high risk of impending cognitive decline because of Alzheimer disease is crucial for successful prevention of dementia. Vascular risk and β-amyloid (Aβ) pathology commonly co-occur in older adults and are significant causes of cognitive impairment.Objective? To determine whether vascular risk and Aβ burden act additively or synergistically to promote cognitive decline in clinically normal older adults; and, secondarily, to evaluate the unique influence of vascular risk on prospective cognitive decline beyond that of commonly used imaging biomarkers, including Aβ burden, hippocampal volume, fludeoxyglucose F18–labeled (FDG) positron emission tomography (PET), and white matter hyperintensities, a marker of cerebrovascular disease.Design, Setting, and Participants? In this longitudinal observational study, we examined clinically normal older adults from the Harvard Aging Brain Study. Participants were required to have baseline imaging data (FDG-PET, Aβ-PET, and magnetic resonance imaging), baseline medical data to quantify vascular risk, and at least 1 follow-up neuropsychological visit. Data collection began in 2010 and is ongoing. Data analysis was performed on data collected between 2010 and 2017.Main Outcomes and Measures? Vascular risk was quantified using the Framingham Heart Study general cardiovascular disease (FHS-CVD) risk score. We measured Aβ burden with Pittsburgh Compound-B PET. Cognition was measured annually with the Preclinical Alzheimer Cognitive Composite. Models were corrected for baseline age, sex, years of education, and apolipoprotein E ε4 status.Results? Of the 223 participants, 130 (58.3%) were women. The mean (SD) age was 73.7 (6.0) years, and the mean (SD) follow-up time was 3.7 (1.2) years. Faster cognitive decline was associated with both a higher FHS-CVD risk score (β?=??0.064; 95% CI, ?0.094 to ?0.033; P??.001) and higher Aβ burden (β?=??0.058; 95% CI, ?0.079 to ?0.037; P??.001). The interaction of the FHS-CVD risk score and Aβ burden with time was significant (β?=??0.040, 95% CI, ?0.062 to ?0.018; P??.001), suggesting a synergistic effect. The FHS-CVD risk score remained robustly associated with prospective cognitive decline (β?=??0.055; 95% CI, ?0.086 to ?0.024; P??.001), even after adjustment for Aβ burden, hippocampal volume, FDG-PET uptake, and white matter hyperintensities.Conclusions and Relevance? In this study, vascular risk was associated with prospective cognitive decline in clinically normal older adults, both alone and synergistically with Aβ burden. Vascular risk may complement imaging biomarkers in assessing risk of prospective cognitive decline in preclinical Alzheimer disease.
机译：重要性？由于阿尔茨海默病，鉴定了迫使认知性下降的高风险的无症状，对于成功预防痴呆至关重要。血管风险和β-淀粉样蛋白（Aβ）病理通常在老年人中共同发生，是认知障碍的重要原因。目的？确定血管风险和Aβ负担是否会加剧或协同作用，以促进临床正常成年人的认知下降;并且，二次，评估血管风险对预期认知衰退的独特影响，超出常用的成像生物标志物，包括Aβ负担，海马体积，氟化葡萄糖F18标记（FDG）正电子发射断层扫描（PET）和白质比度，脑血管疾病的标志。设计，设置和参与者？在这项纵向观察研究中，我们从哈佛大学脑卒中研究检查临床正常的老年人。参与者被要求具有基线成像数据（FDG-PET，Aβ-PET和磁共振成像），基线医疗数据来量化血管风险，至少有1个后续神经心理学访问。数据收集始于2010年并正在进行中。对2010年至2010年至2017年间的数据进行数据分析.Main结果和措施使用Framingham心脏研究综合心血管疾病（FHS-CVD）风险评分量化血管风险。我们用匹兹堡复合-B宠物测量了Aβ负担。通过临床前阿尔茨海默认知复合材料每年测量认知。模型被纠正为基线年龄，性别，年龄的教育和载脂蛋白e∈4状态。结果？在223名参与者中，130名（58.3％）是女性。平均（SD）年龄为73.7（6.0）年，平均（SD）随访时间为3.7（1.2）年。更快的认知下降与较高的FHS-CVD风险评分有关（β？= ?? 0.064; 0.094至0.094至0.033;p≤001）和β致荷（β= ?? 0.058; 95％CI，α079至0.037; p？＆ 001）。 FHS-CVD风险评分的相互作用和随时间的Aβ负担是显着的（β？= ?? 0.040,95％CI，Δ062至Δ018;p≤001），表明协同效应。与前瞻性认知下降（β= 0.055; 95％CI，Δ0.024;p≤00.α.<。001），FHS-CVD风险评分仍然强烈关联FDG-PET吸收，白质比度。结论和相关性吗？在这项研究中，血管风险与临床正常年龄成年人的前瞻性认知下降有关，既单独又与Aβ负担协同增长。血管风险可以补充成像生物标志物，评估临床前阿尔茨海默病的前瞻性认知下降风险。

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