Altered plasma levels of Aβ42/40, different p-tau variants (in particular p-tau217 andp-tau231), and GFAP are increasingly recognized to reflect early Aβ deposition inpreclinical and prodromal stages of AD.12,13 It is reasonable toassume that slow Aβ accumulation seen even in some CU individuals negative forAβ-PET38,39 would also impact plasma biomarker concentrations.However, associations between plasma biomarkers and measures of Aβ pathology in thispopulation are unexplored. Here, GFAP is linked to Alzheimer disease.