Epigenetic Regulation of Amyloid-beta Metabolism in Alzheimer’s Disease

Senile plaques (SPs) are one of the pathological features of Alzheimer’s disease (AD) and they are formed by the overproduction and aggregation of amyloid-beta (Aβ) peptides derived from the abnormal cleavage of amyloid precursor protein (APP). Thus, understanding the regulatory mechanisms during Aβ metabolism is of great importance to elucidate AD pathogenesis. Recent studies have shown that epigenetic modulation—including DNA methylation, non-coding RNA alterations, and histone modifications—is of great significance in regulating Aβ metabolism. In this article, we review the aberrant epigenetic regulation of Aβ metabolism.