Alzheimer disease (AD) is a frequent and devastating neurodegenerative disease in humans, but still no curative treatment has been developed. Although many explicative theories have been proposed, precise pathophysiological mechanisms are unknown. Due to the great importance of astrocytes in brain homeostasis they have become interesting targets for the study of AD. Changes in astrocyte function have been observed in brain tissue from individuals with AD, as well as in AD in vitro and in vivo animal models. Excessive neuroinflammation and oxidative stress are observed in AD and astrocytes seem to be involved in both.Astrocytes participate in the inflammatory/immune responses of the CNS. The presence of amyloidbeta activates different cell receptors and intracellular signaling pathways, mainly the RAGE/NF-κB pathway, responsible for the transcription of pro-inflammatory cytokines and chemokines in astrocytes. The release of these pro-inflammatory agents may induce cellular damage or even stimulate production of amyloid-beta in astrocytes. Amyloid-beta induces the appearance of oxidative stress and production of ROS and RNS in astrocytes, affecting among others, intracellular calcium levels, NADPH oxidase, NF-κB signaling, glutamate uptake (increasing the risk for excitotoxicity) and mitochondrial function. In this paper, we will also discuss therapeutic measures highlighting the importance of astrocytes in AD pathology.