Fig. 2: Sensitivity analyses testing the associations of Aβ-PET and tau-PET with reactive astrocyte biomarkers using plasma GFAP instead of CSF GFAP. | Molecular Psychiatry

Fig. 2: Sensitivity analyses testing the associations of Aβ-PET and tau-PET with reactive astrocyte biomarkers using plasma GFAP instead of CSF GFAP.

From: Astrocyte biomarker signatures of amyloid-β and tau pathologies in Alzheimer’s disease

Fig. 2

A Box-and-whisker plot of plasma GFAP levels adjusted for age, sex, and APOE ε4 status across AT groups. The horizontal line in each box represents the median; box ends represent the 25th and 75th percentiles. Shape of the dots depicts the clinical diagnosis (CU: 73.6% A-T-, and 26.4% A + T−; MCI: 37.0% A − T−, 29.6% A + T−, and 33.3% A + T+; AD: 26.7% A + T−, and 73.3% A + T). Groups were compared using analyses of variance with Tukey’s multiple comparison test (*P < 0.05, **P < 0.01, ***P < 0.001). B Partial residual plots of linear regressions testing the associations of neocortical Aβ-PET SUVR with plasma GFAP and CSF YKL-40 levels adjusting for temporal meta-ROI tau-PET SUVR, age, sex, cognitive status, and APOE ε4 status. The shape of the dots depicts the AT group. C Partial residual plots of linear regressions testing the associations of temporal meta-ROI tau-PET SUVR with plasma GFAP and CSF YKL-40 levels adjusting for neocortical Aβ-PET SUVR, age, sex, cognitive status, and APOE ε4 status. The shape of the dots depicts the AT group. Of note, analyses involving plasma GFAP were conducted in a subset of 114 individuals; from the total study population of 121 subjects, five participants did not have available plasma GFAP measures, and two were excluded because they were considered outliers (plasma GFAP concentrations three SD above the mean of the population). NS not significant.

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