Based on previous literature suggesting an early involvement of neuroinflammation during the AD continuum, we hypothesized that in vivo TSPO binding and plasma GFAP concentrations would be elevated in cognitively normal APOE ε4 homozygotes or APOE ε4 heterozygotes, representing different genetically increased risk for Aβ accumulation and sporadic AD, compared to age-matched non-carriers. This evidence concerns the gene GFAP and Alzheimer disease.