Cellular senescence emerges as a pivotal mechanism accelerating Alzheimer's disease progression through the senescence-associated secretory phenotype (SASP). When brain cells—particularly astrocytes and microglia—enter irreversible growth arrest under stress from amyloid-β toxicity, tau hyperphosphorylation, and oxidative damage, they release proinflammatory factors that destroy mitochondria and disrupt synapses. This mechanistic insight fundamentally reframes Alzheimer's pathology beyond simple protein aggregation to include active cellular aging processes. The therapeutic implications are substantial, positioning senolytics—drugs that eliminate senescent cells—as promising interventions. The review highlights VEGFR-1 and SIRT5 targeting, NLRP3 inflammasome antagonists, and compounds like curcumin derivatives and sildenafil as potential senescence modulators. However, this represents early-stage therapeutic development with limited human clinical validation. The senescence-centric model offers new biomarker opportunities through exosomal analysis and RNA-based interventions. While conceptually compelling, translating anti-senescence strategies from laboratory to clinic remains challenging given the complex role senescent cells play in normal tissue function and the blood-brain barrier's selective permeability.