<![CDATA[The increase in life expectancy is directly proportional to the increasing prevalence of Alzheimer's disease. By 2050, it is estimated that 152 million people will be living with Alzheimer's disease. Alzheimer's disease is a disease caused by progressive neuronal damage, characterized by a decline in cognitive functions such as memory, concentration, and communication impairments. Molecularly, this disease is characterized by the presence of beta-amyloid (Aβ) plaques and tau protein neurofibrillary tangles (NFTs). The pathogenesis of Alzheimer's disease is associated with changes in epigenetic mechanisms, namely changes in DNA expression without involving changes in DNA sequence. Epigenetic mechanisms may contribute to the pathology of Alzheimer's disease through increased activity of the Bace1 and psen1/2 genes, which cleave APP. APP cleavage will predispose to the amyloidogenic pathway, producing toxic Aβ and facilitating tau protein NFTs. The role of epigenetic mechanisms is not limited to the pathology of Alzheimer's disease; several studies have assessed their potential as promising therapeutic targets. Through epigenetic reprogramming, several studies have shown encouraging results. This article reviews the role of epigenetic mechanisms in driving the development of Alzheimer's disease pathology and explores the potential of epigenetic reprogramming as a therapeutic strategy. Through this in-depth approach, it is hoped that this article will open new perspectives on the role of epigenetic mechanisms in Alzheimer's disease pathology and therapeutic targets.]]>
