In models aiming to investigate the independent and interactive effect of plasma GFAP, plasma Aβ42/Aβ40, and plasma p-Tau181 on hippocampal atrophy and AD-signature cortical thinning, we found higher plasma GFAP concentrations (βstd = -0.162[95% ci, -0.288, -0.035], p = 0.012) and APOE-ε4 non-carriers (βstd = -0.363[95% ci, -0.586, -0.141], p = 0.001) were related to more shrinking in temporal-metaROI cortical thickness (Fig. 5A). The gene discussed is GFAP; the disease is hippocampal atrophy.