These results reveal astrocytes' dual role in AD pathogenesis, promoting neuroinflammation through ECM remodeling while simultaneously showing impaired potassium channel function, which disrupts ionic homeostasis and compromises neuronal communication (Liddelow et al., 2017; Akiyama et al., 2000), ultimately accelerating disease progression through multiple converging pathways. This evidence concerns the gene KCNA3 and Alzheimer disease.