GADD45G operates as a pathological sensor orchestrating reactive gliosis and neurodegeneration

Emerging evidence indicates that AD progression is associated with astrocytes transitioning from a homeostatic state to a disease-associated state. This transition is characterized by changes in their morphology, gene expression, and function. We here report GADD45G as a key regulator of the pathogenesis of AD. To determine the role of GADD45G in astrocytes, we conducted unbiased RNA-seq analysis on astrocytes transduced with a virus expressing GADD45G or the control GFP. In addition, we also conducted RNA-seq analysis on astrocytes following shRNA-mediated knockdown of endogenous Gadd45g (shGadd45g).