GFAP and Alzheimer disease: For instance, astrocytes’ close interaction with AD hallmarks (e.g., dystrophic neurites, Aß plaques) can alter their morphology, notably resulting in hypertrophic and atrophic phenotypes (Zhou et al., 2019) as well as their gene and protein expression [e.g., GFAP, serpina3n, aquaporin 4 (AQP4), intercellular adhesion molecule 1 (ICAM-1)] (Akiyama et al., 1993; Orre et al., 2014; Habib et al., 2020; Spanos and Liddelow, 2020; Morabito et al., 2021).