Though Alzheimer’s disease (AD) is a common and fatal neurodegenerative brain disorder, most AD treatments are not making much headway in adressing its cause. Many AD drugs have targeted the elimination of beta-amyloid (Aβ) or amyloid plaques, which block cell-to-cell signaling at synapses. But some AD patients continue to show neurodegeneration and cognitive decline even after the removal of the amyloid plaques. Conversely, many people show no signs of neurodegeneration and cognitive impairment even in very high level of Aβ. Also, it has never been precisely clear as to why the star-shaped non-neuronal cells, called astrocytes, change in their shapes and functions from the early onset of AD, and continue in such reactive states throughout the AD progression.