When using both slopes of plasma p-tau217 and slopes of plasma GFAP simultaneously to predict longitudinal atrophy, plasma p-tau217 remained significant (P = 0.002), while the effect of plasma GFAP was attenuated (P = 0.77), suggesting that plasma GFAP did not contribute as a longitudinal proxy of atrophy beyond the effect of plasma p-tau217 in the early stages of AD. This evidence concerns the gene GFAP and Alzheimer disease.