Age-related neurological disorders represent a major global health challenge due to increasing life expectancy and the growing prevalence of neurodegenerative diseases. Conditions such as Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, Huntington’s disease, and vascular dementia are characterized by progressive neuronal dysfunction and loss, leading to cognitive, motor, and behavioral impairments. Emerging evidence suggests that neuroinflammation is a critical contributor to the initiation and progression of neurodegeneration. Chronic activation of microglia and astrocytes, excessive production of pro-inflammatory cytokines, oxidative stress, mitochondrial dysfunction, and disruption of the blood–brain barrier collectively contribute to neuronal damage. Neuroinflammation, once considered merely a secondary response to neuronal injury, is now recognized as a central pathological mechanism that interacts closely with protein aggregation, synaptic dysfunction, and cellular aging. This review summarizes current knowledge regarding the molecular and cellular mechanisms linking neuroinflammation and neurodegeneration in age-related neurological disorders. Particular emphasis is placed on inflammatory pathways, immune responses, biomarkers, therapeutic targets, and emerging treatment strategies aimed at modulating neuroinflammatory processes. Understanding these complex interactions may facilitate the development of novel interventions to delay disease progression and improve neurological health in aging populations.