18F-Flortaucipir Binding in Choroid Plexus: Related to Race and Hippocampus Signal.

18F-Flortaucipir Binding in Choroid Plexus: Related to Race and Hippocampus Signal.
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DOI:
10.3233/jad-170840
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发表时间:
2018
期刊:
Journal of Alzheimer's disease : JAD
影响因子:
--
通讯作者:
Johnson KA
Johnson KA
中科院分区:
其他
文献类型:
--
作者:
Lee CM;Jacobs HIL;Marquié M;Becker JA;Andrea NV;Jin DS;Schultz AP;Frosch MP;Gómez-Isla T;Sperling RA;Johnson KA

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已经用放射自显影术证明了阿尔茨海默病tau聚集体的靶向18F-氟陶西匹(FTP)结合和黑素细胞的脱靶结合。我们的目的是研究假设,如果脉络丛(CP)中的结合是由于黑素细胞,则与白色(W)参与者相比,黑人/非裔美国人(B/AA)中的信号将升高。此外,我们研究了CP信号是否影响相邻区域的测量,以及校正溢出效应是否影响海马(HC)FTP与淀粉样蛋白或认知之间的关联。研究了147名哈佛老年脑研究参与者(23名B/AA,124 W)的FTP种族差异,包括CP、HC、CP、杏仁核、颞下回、内嗅皮层和梭状区的HC协变。CP FTP和其他感兴趣的区域(ROI)之间的关联进行了探讨,以评估溢出效应。通过将调整后的HC SUVR残差和未调整的HC SUVR与种族、认知和淀粉样蛋白相关,测试了减弱CP溢出的统计回归方法。所有的分析都是年龄、性别、教育和淀粉样蛋白沉积的协变量,并对多重比较进行Bonferroni校正。B/AA个体CP和HC SUVR升高(p < 0.007),而其他ROI SUVR和HC SUVR协变的CP SUVR未显示种族差异(p > 0.05)。CP SUVR与HC SUVR相关(p < 10−14),但与其他ROI SUVR无关(p > 0.05)。当用CP SUVR调整HC SUVR时,未检测到残留HC SUVR的种族差异,并且与淀粉样蛋白和记忆的关系变得明显。黑素细胞FTP结合可能部分地解释高CP信号。这种脱靶结合主要影响HC FTP测量,应谨慎解释。
On target 18F-Flortaucipir (FTP) binding of Alzheimer’s disease tau aggregates and off-target binding of melanocytes have been demonstrated with autoradiography. We aimed to investigate the hypothesis that if binding in choroid plexus (CP) is due to melanocytes, the signal would be elevated in Black/African American (B/AA) compared to White (W) participants. In addition, we examined whether CP signal affects measurements in adjacent regions, and whether correcting for spill-in effects has an influence on associations between hippocampus (HC) FTP and amyloid or cognition. FTP race differences in 147 Harvard Aging Brain Study participants (23 B/AA, 124W) were examined in CP, HC, HC covaried for CP, amygdala, inferior temporal gyrus, entorhinal cortex, and fusiform regions. Associations between CP FTP and other regions-of-interest (ROIs) were probed to assess spill-in effects. A statistical regression approach to attenuate CP spill-in was tested by relating adjusted HC SUVR residuals and unadjusted HC SUVR to race, cognition and amyloid. All analyses were covaried for age, sex, education and amyloid deposition, and Bonferroni-corrected for multiple comparisons. B/AA individuals had elevated CP and HC SUVR (p < 0.007), whereas other ROI SUVR and HC SUVR covaried for CP SUVR did not show race differences (p > 0.05). CP SUVR was associated with HC SUVR (p < 10−14), but with no other ROI SUVR (p > 0.05). When adjusting HC SUVR for CP SUVR, no race differences in residual HC SUVR were detected, and relationships with amyloid and memory became apparent. Melanocyte FTP binding may account partially for high CP signal. This off-target binding affects mainly HC FTP measurements, which should be interpreted with caution.