Senescent brain cells drive a harmful inflammatory cascade that accelerates Alzheimer's pathology through the senescence-associated secretory phenotype (SASP). When glial and neuronal cells accumulate age-related damage, they secrete inflammatory molecules that activate NLRP3 inflammasomes and NF-κB signaling in surrounding microglia and astrocytes, creating a self-reinforcing cycle of neuroinflammation and oxidative stress that promotes amyloid-β buildup and tau pathology. This mechanistic understanding represents a significant advance in Alzheimer's research by identifying cellular senescence as a central driver rather than merely a consequence of brain aging. The discovery positions senolytics—drugs that eliminate senescent cells—as potentially transformative treatments, moving beyond symptomatic approaches to target root causes. However, the therapeutic promise faces substantial hurdles including inconsistent biomarker measurements across studies and poor drug delivery to brain tissue. The field now needs standardized senescence biomarkers and novel delivery systems to translate these insights into clinical reality. This framework suggests Alzheimer's prevention might require intervening in the aging process itself, fundamentally shifting how we approach neurodegenerative disease.