Aging stands as the fundamental factor, which determines Parkinson’s development because the condition produces motor deficits by degenerating dopaminergic neurons in the substantia nigra region. Older cells enter cellular senescence after arresting their cycle, generating this distinctive state with structural and functional alterations that produce pro-inflammatory factors that turn into senescence-associated secretory phenotype (SASP). Neurons, astrocytes, and microglia accelerate PD development by creating oxidative stress in central nervous system tissue and harmful effects related to proteostatic breakdown, sustained inflammation, and mitochondrial damage. When SASP develops from cellular senescence, it enhances neuroinflammatory responses, harms cellular equilibrium, and accelerates the destruction of neurons. PD pathological stimuli, including α-synuclein aggregation and reactive oxygen species, lead to increased senescence frequencies in vulnerable neural cells. The present research evaluates how senescent cells affect PD progression by reviewing animal and human studies and assessing future therapies that utilize senomorphics and senolytics for targeting senescent cells. The discovery of cellular senescence in PD has generated new disease processes that allow researchers to develop promising treatments for delaying or reversing neurodegenerative effects.