In our cohort, composed of relatively young PWH not selected for the presence of AD, APOE \documentclass[12pt]{minimal}\usepackage{amsmath}\usepackage{wasysym}\usepackage{amsfonts}\usepackage{amssymb}\usepackage{amsbsy}\usepackage{mathrsfs}\usepackage{upgreek}\setlength{\oddsidemargin}{-69pt}\begin{document}$$\upvarepsilon$$\end{document}ε4 exerted a pro-inflammatory effect in the immediate plaque microenvironment, associated with greater infiltrates of Iba1- and CD68-expressing microglia as well as GFAP-positive astrocytes (Table 5). The gene discussed is GFAP; the disease is Alzheimer disease.