Given that the onset of abnormal brain Aβ load build-up assessed using PET begins as early as two decades prior to the clinical manifestation of AD, and is a prodromal feature and biomarker of AD2,10, plasma GFAP levels were compared between cognitively normal older adults with low brain Aβ load (Aβ−) and cognitively normal older adults at risk of AD, due to high brain Aβ load, (Aβ+)11. This evidence concerns the gene GFAP and Alzheimer disease.