Subsequently, a person develops the neurodegenerative disease Alzheimer’s disease in which amyloid-β plaques and hyperphosphorylated tau protein neurofibrillary tangles accumulate, thus causing widespread neuronal death and cognitive impairment as well as synaptic loss. The most prevalent type of dementia, known as AD, causes significant public health problems that affect the social economy negatively. Recent medical research indicates cellular senescence is a critical mechanism behind neurodegeneration and brain aging. Stress factors such as oxidative stress, DNA damage, and telomere shortening halt cells permanently in their growth cycle. As brains age, neurons, microglia, and astrocytes become more numerous, revealing senescence-associated secretory phenotype (SASP) characteristics. Cells accumulating in the AD environment produce reactive oxygen species, proinflammatory cytokines, and matrix metalloproteinases, worsening AD pathology and creating sustained neuroinflammation and synapse interruption. Research from human brains after death demonstrates senescent markers within AD-affected regions, whereas laboratory studies prove that discarding senescent cells from AD mouse models leads to better memory functions alongside decreased brain degeneration. The therapeutic application of senomorphics and senolytics shows promise in treating cases of illness by reducing SASP toxicities while restoring tissue balance. The chapter uses current findings from both human and animal subjects to explain how cellular senescence influences AD disease development. The research evaluates therapeutic possibilities that come from modulating senescence through therapeutic approaches. The document builds essential foundational knowledge about this complex biological process to develop new treatment methods, highlighting why translational research aims to modify cellular senescence for AD prevention.