The article reviews the role of cellular senescence in neurodegenerative diseases (NDs), including Alzheimer's disease (AD) and Parkinson's disease (PD). Senescent cells, characterized by high expression of senescence hallmarks (p16 and p21) and elevated β-galactosidase activity, secrete senescence-associated secretory phenotypes (SASPs) such as matrix metalloproteinase-3, interleukins (IL-1α, IL-6, and IL-8), which can harm adjacent microglia and contribute to the deposition of β-amyloid and tau proteins. Selective clearance of senescent cells and regulation of SASP through inhibiting p38/mitogen-activated protein kinase and nuclear factor kappa B signaling can improve cognitive performance in AD mouse models. Telomere shortening, a biomarker of cellular senescence, is associated with increased ND risks and causes cellular senescence, leading to increased secretion of pro-inflammatory cytokines. Telomerase activation prevents cellular senescence and shows neuroprotective effects. The review highlights the mechanisms of cellular senescence in ND pathogenesis and suggests strategies to eliminate or restore senescent cells to treat NDs.The article reviews the role of cellular senescence in neurodegenerative diseases (NDs), including Alzheimer's disease (AD) and Parkinson's disease (PD). Senescent cells, characterized by high expression of senescence hallmarks (p16 and p21) and elevated β-galactosidase activity, secrete senescence-associated secretory phenotypes (SASPs) such as matrix metalloproteinase-3, interleukins (IL-1α, IL-6, and IL-8), which can harm adjacent microglia and contribute to the deposition of β-amyloid and tau proteins. Selective clearance of senescent cells and regulation of SASP through inhibiting p38/mitogen-activated protein kinase and nuclear factor kappa B signaling can improve cognitive performance in AD mouse models. Telomere shortening, a biomarker of cellular senescence, is associated with increased ND risks and causes cellular senescence, leading to increased secretion of pro-inflammatory cytokines. Telomerase activation prevents cellular senescence and shows neuroprotective effects. The review highlights the mechanisms of cellular senescence in ND pathogenesis and suggests strategies to eliminate or restore senescent cells to treat NDs.