Astrocytes that surround amyloid plaques become reactive in Alzheimer disease (AD), but their role in AD pathogenesis is poorly understood. Using a mouse model of AD, Jo et al. have discovered that reactive astrocytes produce abundant γ-aminobutyric acid (GABA). Suppression of aberrant GABA secretion rescued the AD-like impairments in synaptic plasticity, learning, and memory, suggesting that selective inhibition of astrocytic GABA release might alleviate AD.