This review explores the role of DNA methylation and histone modifications in Alzheimer's disease (AD) pathogenesis. Alzheimer's disease is a progressive neurodegenerative disorder characterized by cognitive decline and memory loss. While therapeutic approaches have shown promise, understanding the molecular mechanisms underlying AD remains critical. Epigenetic changes, including DNA methylation and histone modifications, are increasingly recognized as key factors in AD development. These epigenetic alterations influence gene expression patterns associated with AD pathology, such as synaptic plasticity, neuroinflammation, and oxidative stress. The review highlights the dynamic interplay between genetic and environmental factors that shape the epigenetic landscape in AD. DNA methylation involves the addition of methyl groups to DNA, regulated by enzymes like DNMTs, and is associated with changes in gene expression. Histone modifications, such as acetylation, methylation, and phosphorylation, regulate chromatin structure and gene expression. These modifications are linked to AD pathology, including amyloid-beta (Aβ) accumulation and tau pathology. The review also discusses the potential therapeutic applications of targeting these epigenetic mechanisms, including the use of HDAC inhibitors and sirtuins. Despite promising findings, challenges remain in translating these insights into effective treatments due to issues such as off-target effects and limited brain penetration of some drugs. Overall, understanding the epigenetic mechanisms in AD offers new avenues for developing targeted therapeutic strategies.This review explores the role of DNA methylation and histone modifications in Alzheimer's disease (AD) pathogenesis. Alzheimer's disease is a progressive neurodegenerative disorder characterized by cognitive decline and memory loss. While therapeutic approaches have shown promise, understanding the molecular mechanisms underlying AD remains critical. Epigenetic changes, including DNA methylation and histone modifications, are increasingly recognized as key factors in AD development. These epigenetic alterations influence gene expression patterns associated with AD pathology, such as synaptic plasticity, neuroinflammation, and oxidative stress. The review highlights the dynamic interplay between genetic and environmental factors that shape the epigenetic landscape in AD. DNA methylation involves the addition of methyl groups to DNA, regulated by enzymes like DNMTs, and is associated with changes in gene expression. Histone modifications, such as acetylation, methylation, and phosphorylation, regulate chromatin structure and gene expression. These modifications are linked to AD pathology, including amyloid-beta (Aβ) accumulation and tau pathology. The review also discusses the potential therapeutic applications of targeting these epigenetic mechanisms, including the use of HDAC inhibitors and sirtuins. Despite promising findings, challenges remain in translating these insights into effective treatments due to issues such as off-target effects and limited brain penetration of some drugs. Overall, understanding the epigenetic mechanisms in AD offers new avenues for developing targeted therapeutic strategies.