首页> 外文期刊>Journal of Alzheimer's disease: JAD >Modeling the Relationships Among Late-Life Body Mass Index, Cerebrovascular Disease, and Alzheimer's Disease Neuropathology in an Autopsy Sample of 1,421 Subjects from the National Alzheimer's Coordinating Center Data Set
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Modeling the Relationships Among Late-Life Body Mass Index, Cerebrovascular Disease, and Alzheimer's Disease Neuropathology in an Autopsy Sample of 1,421 Subjects from the National Alzheimer's Coordinating Center Data Set

机译:在全国阿尔茨海默协调中心数据集的1,421个科目的尸检样本中建模了晚期体重指数,脑血管疾病和阿尔茨海默病神经病理学的关系

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The relationship between late-life body mass index (BMI) and Alzheimer's disease (AD) is poorly understood due to the lack of research in samples with autopsy-confirmed AD neuropathology (ADNP). The role of cerebrovascular disease (CVD) in the interplay between late-life BMI and ADNP is unclear. We conducted a retrospective longitudinal investigation and used joint modeling of linear mixed effects to investigate causal relationships among repeated antemortem BMI measurements, CVD (quantified neuropathologically), and ADNP in an autopsy sample of subjects across the AD clinical continuum. The sample included 1,421 subjects from the National Alzheimer's Coordinating Center's Uniform Data Set and Neuropathology Data Set with diagnoses of normal cognition (NC; n = 234), mild cognitive impairment MCI; n = 201), or AD dementia (n = 986). ADNP was defined as moderate to frequent neuritic plaques and Braak stage III-VI. Ischemic Injury Scale (IIS) operationalized CVD. Joint modeling examined relationships among BMI, IIS, and ADNP in the overall sample and stratified by initial visit Clinical Dementia Rating score. Subject-specific random intercept for BMI was the predictor for ADNP due to minimal BMI change (p = 0.3028). Analyses controlling for demographic variables and APOE epsilon 4 showed lower late-life BMI predicted increased odds of ADNP in the overall sample (p < 0.001), and in subjects with CDR of 0 (p = 0.0021) and 0.5 (p = 0.0012), but not >= 1.0 (p = 0.2012). Although higher IIS predicted greater odds of ADNP (p < 0.0001), BMI did not predict IIS (p = 0.2814). The current findings confirm lower late-life BMI confers increased odds for ADNP. Lower late-life BMI may be a preclinical indicator of underlying ADNP.
机译:由于具有尸检确认的AD神经病理学(ADNP)的样品缺乏研究,晚寿命体重指数(BMI)和阿尔茨海默病(AD)之间的关系差不多理解。脑血管疾病(CVD)在晚期生活BMI和ADNP之间的相互作用中的作用尚不清楚。我们进行了回顾性的纵向调查,并使用了线性混合效应的联合建模,以研究反复抗emortemBMI测量,CVD(定量神经病理学)中的因果关系,以及在AD临床连续体中的受试者的尸检样本中的ADNP。该样本包括来自国家阿尔茨海默氏症的协调中心的统一数据集和神经病理学数据集的1,421个受试者,具有正常认知(NC; N = 234)的诊断,轻度认知障碍MCI; n = 201),或广告痴呆(n = 986)。 ADNP被定义为中等至频繁的神经斑块和BRAAK阶段III-VI。缺血性损伤量表(IIS)业务化CVD。联合建模在整体样本中BMI,IIS和ADNP中的关系检查,并通过初次访问临床痴呆评分分层分层。 BMI的主题特定随机截距是由于最小的BMI变化导致ADNP的预测器(P = 0.3028)。分析控制人口变量和Apoe epsilon 4显示出较低的后期BMI预测整个样品中的ADNP的差异增加(P <0.001),以及CDR的受试者(p = 0.0021)和0.5(p = 0.0012),但不是> = 1.0(p = 0.2012)。虽然更高的IIS预测ADNP的少量差异(P <0.0001),但BMI没有预测IIS(P = 0.2814)。目前的调查结果确认了较低的后期BMI赋予ADNP的赔率增加。下寿命的后期BMI可能是底层ADNP的临床前指标。

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