PURPOSE [18F]FDG-PET and [11C]PIB-PET are validated as neurodegeneration and amyloid biomarkers of Alzheimer's disease (AD). We used a PET staging system based on the 2018 NIA-AA research framework to compare the proportion of amyloid positivity (A+) and hypometabolism ((N)+) in cases of mild probable AD, amnestic mild cognitive impairment (aMCI), and healthy controls, incorporating an additional classification of abnormal [18F]FDG-PET patterns and investigating the co-occurrence of such with A+, exploring [18F]FDG-PET to generate hypotheses in cases presenting with clinical-biomarker "mismatches." METHODS Elderly individuals (N = 108) clinically classified as controls (N = 27), aMCI (N = 43) or mild probable AD (N = 38) were included. Authors assessed their A(N) profiles and classified [18F]FDG-PET neurodegenerative patterns as typical or non-typical of AD, performing re-assessments of images whenever clinical classification was in disagreement with the PET staging (clinical-biomarker "mismatches"). We also investigated associations between "mismatches" and sociodemographic and educational characteristics. RESULTS AD presented with higher rates of A+ and (N)+. There was also a higher proportion of A+ and (N)+ individuals in the aMCI group in comparison to controls, however without statistical significance regarding the A staging. There was a significant association between amyloid positivity and AD (N)+ hypometabolic patterns typical of AD. Non-AD (N)+ hypometabolism was seen in all A- (N)+ cases in the mild probable AD and control groups and [18F]FDG-PET patterns classified such individuals as "SNAP" and one as probable frontotemporal lobar degeneration. All A- (N)- cases in the probable AD group had less than 4 years of formal education and lower socioeconomic status (SES). CONCLUSION The PET-based staging system unveiled significant A(N) differences between AD and the other groups, whereas aMCI and controls had different (N) staging, explaining the cognitive impairment in aMCI. [18F]FDG-PET could be used beyond simple (N) staging, since it provided alternative hypotheses to cases with clinical-biomarker "mismatches." An AD hypometabolic pattern correlated with amyloid positivity. Low education and SES were related to dementia in the absence of biomarker changes.

中文翻译：

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在2018 NIA-AA研究框架的背景下，大脑PET淀粉样蛋白和神经变性生物标记物：探索临床生物标记物不匹配和社会人口统计学参数的单独方法。

目的[18F] FDG-PET和[11C] PIB-PET被证实可作为阿尔茨海默氏病（AD）的神经变性和淀粉样生物标志物。我们使用了基于2018年NIA-AA研究框架的PET分期系统，比较了轻度可能AD，轻度轻度认知障碍（aMCI）和健康情况下淀粉样蛋白阳性（A +）和低代谢（（N）+）的比例对照，结合异常[18F] FDG-PET模式的其他分类，并研究此类异常与A +的共存情况，探索[18F] FDG-PET在临床生物标志物“不匹配”的病例中产生假设。方法包括临床上分为对照组（N = 27），aMCI（N = 43）或轻度可能的AD（N = 38）的老年人（N = 108）。作者评估了他们的A（N）资料，并将[18F] FDG-PET神经退行性疾病分类为AD的典型或非典型，只要临床分类与PET分期不一致（临床生物标志物“不匹配”），就对图像进行重新评估。 ）。我们还研究了“错配”与社会人口统计学和教育特征之间的关联。结果AD呈现更高的A +和（N）+比率。与对照组相比，aMCI组中的A +和（N）+个体比例也更高，但是关于A分期没有统计学意义。淀粉样蛋白阳性与AD典型的AD（N）+代谢模式之间存在显着关联。在轻度可能的AD和对照组中，在所有A-（N）+病例中均观察到非AD（N）+代谢不足，[18F] FDG-PET模式将此类个体归类为“ SNAP”，其中一个被分类为额颞叶变性。在可能的AD组中，所有A-（N）-病例的正规教育少于4年，社会经济地位（SES）较低。结论基于PET的分期系统揭示了AD与其他组之间的显着A（N）差异，而aMCI和对照具有不同的（N）分期，这解释了aMCI的认知障碍。[18F] FDG-PET可以用于简单的（N）分期，因为它为具有临床生物标志物“不匹配”的病例提供了其他假设。AD低代谢模式与淀粉样蛋白阳性相关。