Astrocytes are thought to play a protective role in Alzheimer's disease (AD) by shielding neurons from the toxic effects of extracellular senile plaques. The mechanisms involved in the recruitment of astrocytes to senile plaques are unclear, and studies examining the astrocyte response to extracellular beta-amyloid (Abeta) are limited. However, recent work has shown that astrocytes migrating towards monocyte chemoattractant protein-1 become immobilized when they encounter Abeta. Once in the presence of Abeta, astrocytes can internalize and degrade it. It is possible that this proposed function for astrocytes is inactivated or overwhelmed in AD.