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. 2022 Mar 28;14:771214. doi: 10.3389/fnagi.2022.771214

Table 4.

Comparison of the effect of APOE ε4 status and brain Aβ status on plasma Aβ1−42 levels and blood biomarker ratios.

APOE ε4 status
1−42 ε4– ε4+ p(F)# pa(Fa)#
All 0.337 ± 0.077 0.308 ± 0.068 0.013 (6.297) 0.031 (4.746)
APP669−711/Aβ1−42 ε4– ε4+ p(F) pa(Fa)
All 0.839 ± 0.131 0.943 ± 0.139 <0.001 (19.936) <0.001 (15.129)
1−40/Aβ1−42 ε4– ε4+ p(F) pa(Fa)
All 25.10 ± 3.62 27.22 ± 3.72 0.001 (11.077) <0.001 (14.582)
Brain Aβ status
1−42 Aβ- Aβ+ p(F)# pa(Fa)#
All 0.343 ± 0.077 0.305 ± 0.068 0.001 (11.733) 0.001 (11.876)
APP669−711/Aβ1−42 Aβ- Aβ+ p(F) pa(Fa)
All 0.811 ± 0.117 0.963 ± 0.128 <0.001 (54.898) <0.001 (54.199)
1−40/Aβ1−42 Aβ- Aβ+ p(F) pa(Fa)
All 24.38 ± 3.47 27.83 ± 3.28 <0.001 (36.509) <0.001 (36.304)

Plasma Aβ1−42 and the ratios APP669−711/Aβ1−42 and Aβ1−40/Aβ1−42 were compared with regards to APOE ε4 genotype status (ε4–/ε4+), and brain amyloid status (Aβ-/+) using general linear models. Brain amyloid deposition was measured using positron emission tomography. Plasma Aβ1−42 data were natural log transformed to better approximate normality and variance homogeneity (#). pa(Fa) represents p-values adjusted for age and sex. P < 0.05 (italic) was considered significant. Data are presented in mean ± SD.