Amyloid and tau‐driven signatures in hippocampal GFAP‐positive astrocytes

Despite the known heterogeneity of astrocyte responses to injuries, Alzheimer’s disease (AD) pre‐clinical and clinical research relies on the glial fibrillary acidic protein (GFAP) as a proxy of astrocyte reactivity. Recently, it was demonstrated that plasma GFAP levels differentially relate to AD hallmarks, associating with amyloid‐β (Aβ), but not with tau pathology. However, the molecular underpinnings behind this specificity are still unexplored. Here, we aim to uncover the molecular signatures of GFAP‐positive astrocytes driven by either by Aβ or tau pathology.