Cellular senescence plays a critical role in neurodegenerative diseases (NDs), including Alzheimer's disease (AD) and Parkinson's disease (PD). Senescent cells secrete senescence-associated secretory phenotypes (SASP), which contribute to neuroinflammation and the accumulation of β-amyloid and tau protein tangles. These cells express high levels of senescence hallmarks, such as p16 and p21, and their clearance can reduce β-amyloid load and improve cognitive function in AD models. Telomere shortening, a marker of cellular senescence, is associated with increased ND risk and can be mitigated by telomerase activators, which have neuroprotective effects. Cellular senescence is linked to various NDs, including AD, PD, and Huntington's disease, and its accumulation contributes to neurodegeneration. Targeting senescent cells through senolytics or senomorphics can alleviate ND symptoms by reducing SASP and inflammation. Research indicates that eliminating senescent cells improves cognitive function and reduces neurodegeneration in animal models. However, challenges remain in translating these findings to clinical applications, including the need for more effective therapies and a deeper understanding of the molecular mechanisms involved. Future studies should focus on developing targeted interventions to treat NDs by addressing cellular senescence.Cellular senescence plays a critical role in neurodegenerative diseases (NDs), including Alzheimer's disease (AD) and Parkinson's disease (PD). Senescent cells secrete senescence-associated secretory phenotypes (SASP), which contribute to neuroinflammation and the accumulation of β-amyloid and tau protein tangles. These cells express high levels of senescence hallmarks, such as p16 and p21, and their clearance can reduce β-amyloid load and improve cognitive function in AD models. Telomere shortening, a marker of cellular senescence, is associated with increased ND risk and can be mitigated by telomerase activators, which have neuroprotective effects. Cellular senescence is linked to various NDs, including AD, PD, and Huntington's disease, and its accumulation contributes to neurodegeneration. Targeting senescent cells through senolytics or senomorphics can alleviate ND symptoms by reducing SASP and inflammation. Research indicates that eliminating senescent cells improves cognitive function and reduces neurodegeneration in animal models. However, challenges remain in translating these findings to clinical applications, including the need for more effective therapies and a deeper understanding of the molecular mechanisms involved. Future studies should focus on developing targeted interventions to treat NDs by addressing cellular senescence.