Alzheimer's disease (AD) stands as a prevalent and debilitating neurodegenerative disorder, primarily affecting the aging population. It is characterized by a progressive decline in cognitive function, prominently manifesting as memory loss, ultimately leading to dementia. The neuropathological hallmarks of AD include the extracellular accumulation of amyloid-beta (Aβ) plaques and the intracellular formation of neurofibrillary tangles (NFTs) composed of hyperphosphorylated tau protein. Despite extensive research efforts, current therapeutic interventions for AD remain limited, primarily offering symptomatic relief without effectively halting or reversing the underlying disease progression. This limitation underscores the urgent need for the development of novel therapeutic strategies that target the fundamental mechanisms driving AD. Increasingly, the scientific community recognizes glial cells, particularly astrocytes, as crucial players in the initiation and progression of AD pathology. While the amyloid cascade hypothesis, focusing on Aβ and tau, has long dominated AD research, the limited success of treatments targeting these pathologies has prompted a broader investigation into the roles of other cellular components within the brain. The growing body of evidence implicating astrocytes in various aspects of AD pathogenesis positions them as promising targets for future research and the development of more effective therapeutic interventions.

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