Aging is characterized by changes in cellular identity and function over time, with alterations in epigenetic patterns potentially serving as an underlying mechanism that drives human aging. Recent studies have identified sets of individual methylation sites, whose combined DNA methylation status serves as a measure of chronological age, known as the DNA methylation clock. These sites, highly enriched in Polycomb repressive complexes binding locations and associated with chromatin factor localization, are located near genes implicated in mammalian development and longevity. Age-related alterations in the human DNA methylome are believed to contribute to age-related diseases, including neurodegenerative diseases. The two most common neurodegenerative diseases, Alzheimer’s disease (AD) and Parkinson’s disease (PD), arise from a combination of genetic and environmental factors, with aging being a significant risk factor. DNA methylation changes are among the key hallmarks of neurodegeneration, reflecting both the aging process and environmental influences. In AD, DNA methylation aging accelerates as the disease advances, while in PD, accelerated aging correlates with earlier onset. Widespread epigenetic dysregulation is linked to neurodegenerative changes through accelerated aging and pathogenesis in AD and PD. In this chapter, we explore the intricate relationship between DNA methylation changes, aging, and neurodegenerative diseases.