Alzheimer’s disease (AD) involves progressive neurodegeneration, characterized by cognitive decline and accumulation of β-amyloid protein (Aβ) and neurofibrillary tangles (NFTs). Neuroinflammation, driven by microglia and astrocytes, plays a crucial role in AD pathogenesis. Microglia phagocytose Aβ but can exacerbate disease if overactivated. Astrocytes, though protective, can contribute to neuroinflammation and Aβ production when reactive. Current treatments, including monoclonal antibodies targeting Aβ, show promise but do not reverse disease. Future research aims to mitigate neuroinflammation and enhance protective microglia-astrocyte interactions for potential AD therapies.