Neuroinflammation is increasingly recognized as a pivotal factor in the pathogenesis of Alzheimer’s disease (AD), a neurodegenerative disorder characterized by amyloid-beta plaques and tau neurofibrillary tangles. Traditionally viewed as a secondary response to neuronal damage, recent research suggests that neuroinflammation actively contributes to both the initiation and progression of AD. Key mediators of neuroinflammation are glial cells, particularly microglia and astrocytes. When persistently activated, these cells release pro-inflammatory cytokines such as interleukin-1β (IL-1β) and tumor necrosis factor-alpha (TNF-α), exacerbating neuronal injury and promoting cognitive decline. Additionally, dysfunction of the blood-brain barrier permits peripheral immune cells to infiltrate the central nervous system, amplifying the inflammatory response and accelerating disease progression. The intricate interplay between neuroinflammation and AD pathology underscores the potential of targeting inflammatory processes as a therapeutic strategy. Current approaches involve anti-inflammatory agents, modulation of microglial activation states, and lifestyle interventions aimed at reducing systemic inflammation. Emerging therapies focus on targeted interventions, including monoclonal antibodies against pro-inflammatory mediators and inhibitors of inflammasome activation. Nonetheless, significant challenges remain, such as delineating the precise mechanisms by which neuroinflammation influences AD pathology and identifying optimal timing for therapeutic intervention. Addressing these challenges is critical for advancing treatment options by mitigating the detrimental effects of chronic neuroinflammation on neurodegeneration. Future research should concentrate on elucidating the mechanistic pathways of neuroinflammation in AD, developing targeted anti-inflammatory therapies, and enhancing early diagnostic capabilities through reliable biomarkers, ultimately aiming to alleviate the profound impact of this debilitating disease.