Astrocytes undergo morphological and functional alterations in several neurological disorders, including Alzheimer’s disease (AD). Using the McGill-R-Thy1-APP rat model, which expresses human AβPP with Swedish and Indiana mutations, we investigated astrocytic morphology and homeostatic functions at 3, 7, 13, and 20 months. Early changes were observed at 3 months, before plaque formation, and persisted across ages with distinct phenotypes: young animals showed reactive GFAP+ astrocytes with extended processes, whereas older animals displayed atrophy. At 13 months, Sholl analysis identified three astrocytic populations defined by distance to Aβ plaques (on-plaque, periplaque, distant), with greater complexity near plaques. Immunohistochemistry showed reduced glutamine synthetase (GS) and aquaporin-4 (AQP4) near plaques, indicating impaired homeostatic functions, while the stress marker MAFG did not increase. Barnes Maze testing at 4 months revealed no significant group differences, although Tg homozygous animals exhibited distinct profiles versus WT. At 12 months, no differences were found between heterozygous and homozygous animals. These findings show that astrocytes undergo early and plaque-associated alterations, with impaired GS- and AQP4-mediated functions in the absence of overt inflammatory upregulation, suggesting a temporally and spatially regulated role of astrocytic dysfunction in AD pathology. Support: PUE2018, UBACYT, PICT 2019-0851/2021-0760.