Neurodegenerative diseases (NDDs), including Alzheimer’s Disease (AD), Parkinson’s Disease (PD), Huntington’sDisease (HD), and Amyotrophic lateral sclerosis (ALS), are characterized by detrimental, chronic neuroinflammation primarilygenerated by the aberrant inflammatory response of microglia, the resident immune cells of the brain. The inflammatory signatureof microglia is mediated by pro-inflammatory cytokines, including Interleukin 1beta (IL-1ß). Although upregulated IL-1ß isspeculated to be a key component of microglia’s aberrant immune response in NDDs, the mechanisms causing IL-1ß upregulationare unclear; however, alterations in the microglial epigenetic profile are emerging as a possible contributor to increased IL-1ß.This review summarizes updated discoveries on the role of epigenetic alterations in influencing microglial IL-1ß pathways inNDDs. It specifically focuses on elucidating the impact of microRNAs, histone acetylation agents, histone methylation agents,and DNA methylation agents on the inflammatory profile of microglia. The findings summarized below emphasize epigeneticsas a key component of neuroinflammation in NDDs and suggest that future therapeutic developments target the dysregulationof epigenetic agents in microglia

‍