Neuroinflammation has arisen as a key factor in the pathophysiology of Alzheimer’s disease (AD). Chronic immune activation in the brain leads to the release of pro-inflammatory cytokines and other inflammatory mediators that contribute to neuronal damage, thus impacting cognitive function during the progression of the disease. Transcriptomic and epigenomic analyses were performed to understand the epigenetic mechanisms behind the expression of inflammatory genes in AD brain.