Analysis of 269 studies spanning two decades reveals cellular senescence as a central mechanism driving Alzheimer's, Parkinson's, ALS, and Huntington's diseases. The research identifies senescent microglia—aged brain immune cells—as critical culprits that perpetuate chronic neuroinflammation through their senescence-associated secretory phenotype (SASP). Abnormal tau protein accumulation appears to both trigger and sustain this senescent state, creating destructive feedback loops. This mechanistic convergence represents a paradigm shift in neurodegeneration research. Rather than viewing these diseases as distinct entities with separate pathologies, the evidence points toward shared senescence pathways that could be therapeutically targeted. The emergence of multi-target senomorphics—compounds that modulate rather than eliminate senescent cells—offers unprecedented therapeutic potential. These agents could theoretically address multiple neurodegenerative conditions simultaneously by dampening harmful SASP factors while preserving beneficial senescent cell functions. However, the field faces significant translational hurdles. Most senotherapeutic research remains preclinical, and the blood-brain barrier poses delivery challenges. The bibliometric surge since 2018 suggests accelerating interest, but clinical validation of senescence biomarkers and targeted interventions for brain-specific applications remains largely uncharted territory requiring substantial investment and innovation.