Furthermore, upregulation in REST reduces astrocyte reactivity through repression of inflammatory markers that segregate astrocytes into a reactive subpopulation, thus preventing neuroinflammation-induced reactive cells from populating the brain and exerting neurotoxic effects in human induced pluripotent stem cell (hiPSC)-derived astrocytes from patients with Down syndrome, a condition associated with early-onset AD (Huang et al., 2025). This evidence concerns the gene REST and Alzheimer disease.