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首页> 外文期刊>Neurology. Clinical practice. >Association of Performance on the Financial Capacity Instrument-Short Form With Brain Amyloid Load and Cortical Thickness in Older Adults
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Association of Performance on the Financial Capacity Instrument-Short Form With Brain Amyloid Load and Cortical Thickness in Older Adults

机译:金融协会的性能能力Instrument-Short形成大脑淀粉样蛋白加载和皮质厚度在老年人

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Background and Objectives To investigate the association of the Financial Capacity Instrument-Short Form (FCI-SF) performance and timing total scores with brain beta-amyloid and cortical thickness in cognitively unimpaired (CU) (at baseline) older adults. Methods A total of 309 participants (aged 70 years or older) of the Mayo Clinic Study of Aging underwent C-11-Pittsburgh compound B PET amyloid imaging and MRI, and completed the FCI-SF. Abnormal amyloid PET was defined as standardized uptake value ratio >= 1.48 in an Alzheimer disease (AD)-related region of interest and reduced AD signature cortical thickness as <= 2.68 mm (neurodegeneration). A cohort of 218 (of the 309) participants had follow-up visits (every 15 months) with FCI-SF data for longitudinal analysis (number of visits including baseline, median [range]: 2 [2-4]). In the analysis, we used linear regression and mixed-effects models adjusted for age, sex, education, apolipoprotein E epsilon 4 allele status, global cognitive z score, and previous FCI-SF testing. Results Participants' mean age (SD) was 80.2 (4.8) years (56.3% male individuals). In cross-sectional analysis, abnormal amyloid PET (vs normal) was associated with a lower FCI-SF total score and slower total composite time. In longitudinal analysis, FCI-SF total score declined faster (difference in annualized rate of change, beta coefficient [beta] [95% confidence interval (CI)] = -1.123 [-2.086 to -0.161]) and FCI-SF total composite time increased faster (difference in annualized rate of change, beta [95% CI] = 16.274 [5.951 to 26.597]) for participants with neurodegeneration at baseline (vs those without). Participants who exhibited both abnormal amyloid PET and neurodegeneration at baseline had a greater increase in total composite time when compared with the group without abnormal amyloid and without neurodegeneration (difference in annualized rate of change, beta [95% CI] = 16.750 [3.193 to 30.307]). Discussion Performance and processing speed on the FCI-SF were associated with imaging biomarkers of AD pathophysiology in CU (at baseline) older adults. Higher burdens of imaging biomarkers were associated with longitudinal worsening on FCI-SF performance. Additional research is needed to delineate further these associations and their predictive utility at the individual person level.
机译:调查背景和目标协会的财务能力Instrument-Short (FCI-SF)性能和形式时间与大脑β-淀粉样蛋白和总得分在认知没有皮质厚度(铜)(基线)老年人。309名参与者(70岁或以上的老人)梅奥诊所的研究衰老了C-11-Pittsburgh复合B宠物淀粉样蛋白成像和MRI,完成了FCI-SF。淀粉样宠物被定义为标准化的吸收值率> = 1.48阿尔茨海默病(广告)-相关地区的利益和减少广告签名皮质厚度< = 2.68毫米(神经退化)。参与者后续访问(每15个月)与FCI-SF纵向数据分析(许多访问包括基线,中位数(范围):2[2 - 4])。使用线性回归和mixed-effects模型调整年龄、性别、教育、载脂蛋白ε4等位基因状态,全球认知z分数,和以前的FCI-SF测试。参与者的平均年龄(SD)是80.2(4.8)年(男性个人56.3%)。分析,异常淀粉样宠物(vs正常)FCI-SF总分和较低有关总复合时间慢。分析,FCI-SF总分下降得更快(折合成年率的差异变化,β系数(β)[95%可信区间(CI)]= -1.123(-2.086 - -0.161))和FCI-SF总数复合时间增加更快(差异折合成年率变化,β(95%置信区间)= 16.274参与者的[5.951 - 26.597])神经退化在基线(对那些没有)。参与者表现出异常的淀粉样蛋白在基线有宠物和神经退行性变的大增加总复合的时候相比之下,没有异常的淀粉样蛋白和没有神经退化(差异折合成年率变化,β(95%置信区间)= 16.750[3.193 - 30.307])。处理速度在FCI-SF有关广告病理生理学成像生物标志物铜(基线)老年人。成像生物标志物是相关联的纵向对FCI-SF性能恶化。需要额外的研究来描述这些协会和他们的预测工具在个人层面上。

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