Are there ethnic differences in brain amyloid and tau in the seventh decade of life?

我们的目标是检查人种和种族差异在脑淀粉样蛋白β(Aβ)和主要 阿尔茨海默病(AD)的神经病理成分，解释了已报道的阿尔茨海默病患者痴呆的种族差异 曼哈顿北部的阿尔茨海默氏症我们将研究Aβ和tau脑中的种族差异， 用正电子发射断层扫描(PET)在体内确定，在西班牙裔、非西班牙裔黑人(黑人)、 和来自曼哈顿北部、年龄在60到69岁之间的非西班牙裔白人(白人)。我们还将探索是否 种族差异在脑Aβ和tau解释种族差异的记忆表现，最早的临床 阿尔茨海默病的标志物；种族是否改变载脂蛋白E-ε4与脑Aβ的关系；种族差异是否 识字和脑血管疾病缓和脑A、β和tau与记忆的联系 性能。最后，我们将探讨DAT的高风险是否可归因于高血糖(糖尿病前期 和2型糖尿病)在黑人和西班牙裔与白人之间的比较是由更高的大脑Aβ和 陶先生。与白人相比，曼哈顿北部的老年黑人和西班牙裔患DAT的风险更高。它 尚不清楚这种差异是由于AD神经病理、心血管疾病、心血管疾病危险因素还是社会因素的差异所致 健康决定因素(SDOH)。关于黑人和西班牙裔AD生物标记物的研究还很少 这个问题，特别是在中年后期。我们建议利用知识中的这些差距来解决这些问题 一项正在进行的β和tau PET的资助研究(1R01AG050440，3R01AG050440-02S1；09/01/15-05/31/20) 100名拉美裔美国人，年龄在60岁到69岁之间，是脑部成像的关键期 AD神经病理学。我们建议将这一资助项目扩大到100名60岁至69岁的黑人和白人 来自同一个社区，以便比较黑人、西班牙裔和美国人之间的大脑Aβ、tau、心血管疾病和认知 在这个被忽视的年龄段中的白人。我们将使用18F-Florbetaben PET确定脑Aβ，并使用18F-Tau确定tau。 TK-5351PET在两个时间点相隔24个月。我们还将进行脑部磁共振成像(MRI) 用于PET的联合注册和确定CVD(白质高信号和脑梗塞)。我们的初选 目的是检验全脑纤维Aβ和tau的存在是否存在种族差异。 在黑人、西班牙裔和西班牙裔美国人中，横截面和纵向的内侧颞叶和下颞叶皮质 来自曼哈顿北部社区的60岁至69岁的白人。我们还将探索跨越和内部 各民族全脑纤维Aβ和Tau在内侧颞叶和颞下皮质的相关性， 记忆表现，并通过脑血管疾病和识字来调节这种联系。次要目标1是 跨种族比较载脂蛋白E-ε4与全脑纤维蛋白A、β和tau的相关性 而且是纵向的。第二个目标是探索高血糖的种族差异是否可以解释种族差异。 全脑纤维Aβ、内侧颞叶皮质和颞叶下皮质tau与记忆功能障碍有关。

Our goal is to examine whether ethnic and racial differences in brain amyloid β (Aβ) and tau, the major neuropathology components of Alzheimer’s disease (AD), explain reported ethnic disparities in dementia of the Alzheimer’s type (DAT) in Northern Manhattan We will examine ethnic differences in brain Aβ and tau, ascertained in-vivo with positron emission tomography (PET), among Hispanics, Non-Hispanic Blacks (Blacks), and Non-Hispanic Whites (Whites) aged 60 to 69 years from Northern Manhattan. We will also explore whether ethnic differences in brain Aβ and tau explain ethnic differences in memory performance, the earliest clinical marker of AD; whether ethnicity modifies the relation of APOE-ε4 and brain Aβ; whether ethnic disparities in literacy and cerebrovascular disease (CVD) moderate the association of brain Aβ and tau with memory performance. Lastly, we will explore whether the higher risk of DAT attributable to hyperglycemia (pre-diabetes and type 2 diabetes) among Blacks and Hispanics compared with Whites is explained by higher brain Aβ and tau. The risk of DAT is higher in elderly Blacks and Hispanics in Northern Manhattan compared with Whites. It is unknown whether this disparity is due to differences in AD neuropathology, CVD, CVD risk factors, or social determinants of health (SDOH). There is a paucity of studies of AD biomarkers in Blacks and Hispanics to answer this question, particularly in late middle age. We propose to address these gaps in knowledge taking advantage of an ongoing funded study of Aβ and tau PET (1R01AG050440, 3R01AG050440-02S1;09/01/15-05/31/20) in 100 Hispanics between 60 and 69 years of age at the time of brain imaging, a critical period for accumulation of AD neuropathology. We propose to extend this funded project to 100 Blacks and Whites aged 60 to 69 years from the same community in order to compare brain Aβ, tau, CVD, and cognition among Blacks, Hispanics and Whites in this understudied age group. We will ascertain brain Aβ using 18F-Florbetaben PET, and tau using 18F- THK-5351 PET at 2 time points 24 months apart. We will also conduct brain magnetic resonance imaging (MRI) for co-registration of PET and for ascertainment of CVD (white matter hyperintensities and infarcts). Our primary aim is to examine whether there are ethnic differences in the presence of whole brain fibrillar Aβ, and tau in medial temporal and inferior temporal cortex, cross-sectionally and longitudinally, among Blacks, Hispanics and Whites aged 60 to 69 years from the community of Northern Manhattan. We will also explore across and within ethnic groups the association of whole brain fibrillar Aβ, and tau in medial temporal and inferior temporal cortex, with memory performance, and moderation of this association by CVD and literacy. Secondary aim 1 is to compare the association of APOE-ε4 with whole brain fibrillar Aβ and tau across ethnic groups cross sectionally and longitudinally. Secondary aim 2 is to explore if ethnic disparities in hyperglycemia explain ethnic differences in whole brain fibrillar Aβ, and tau in medial temporal and inferior temporal cortex and memory impairment.