Our study on cognitively unimpaired “at-risk” individuals carrying either one or two copies of the APOE ε4 gene showed clear differences in fibrillar Aβ load in the brain, but the changes were not accompanied by higher glial reactivity as measured with TSPO PET either in APOE ε4 carriers, or in Aβ-positive individuals, representing preclinical AD. This evidence concerns the gene APOE and Alzheimer disease.